Hematology = Red; Leukemia=blue; norm phys=orange; neuro= pink; green=GI; musculoskeletal= purple; liver = teal; sex = maroon INTRO hemoglobin= iron + O2, heme= iron + 4 porforin, globin=
protein (4 parts, 2 alpha, 2 beta) leukopenia: ↓WBC- not norm leukocytosis: norm infection or stress Th count: under 1000- ↑risk infection, under 500- HIV→AIDS ERYTHROCYTE PRODUCTION
uncommitted pluripotent stem cell (become any blood cell) - EPO tells it to become RBC→ committed proerythroblast→ nomoblast (nucleus shrinks & reabsorbed) →reticulocyte (leaves marrow &
enters bloodstream, still have mRNA& ribosomes, live 1 day) →erythrocyte 100-120 days (cell achieves final shape & size, hemoglobin synthesis ceases, no more mRNA or ribosomes); spleen:
lymph node for blood, old RBCs eaten by macrophages in red pulp PROGRESSION OF ANEMIA ↓ O2 carrying capacity in blood; etiologic event ↓ RBCs →↓ hemoglobin →↓ability to transport
O2→hypoxia (↓O2 content) → weakness, fatigue, pallor, ↑ resp rate; compensation for ↓hemoglobin: ↑EPO production  RBCs, ↑ resp but norm O2 sat so out of breath, ↑HR &SV, ↑ECF, move
hemoglobin faster→ cardiac murmurs & high-output cardiac failure, no time for O2 exchange in tissues; TYPES OF ANEMIA MCV: avg vol of RBC macrocytic-normochromic: [MCV>100fL]
megablastic anemia, prob w/ DNA synthesis (slow- cell continues to grow until DNA replication complete); causes: b12 deficiency: impaired DNA synthesis, cells get bigger faster than we can
copy DNA; pernicious amemia: lack of IF, usually carries B12 through GI tract, usually due to autoimmune disease; folate deficiency- common in alcoholics (alcohol ↑ risk of breast cancer bc it
↓folate); drugs that inhibit DNA synthesis (chemo, reverse transcriptase inhibitors); microcytic-hypochromic: [MCV<80fL] problem w/ hemoglobin synthesis, small pale RBCs (w/ some dark RBCs dt
blood transfusion); causes: iron deficiency; lead poising (lead inhibits production of porphyrin) sideroblastic anemia- defect in iron handling (can’t combine w/ porphyrin ring)→dysfunctional
hemoglobin; vitamin B6 deficiency; anemia of chronic disease- attempt to keep iron away from bacteria, sequester it, thalassemia- genetic defect in α-globin or
β- globin, genetic typical of S. Euros, MEasterners, S. Asians; Normocytic-normochromic: normal sized cells with normal amts of hemoglobin; ↓ RI- not making
enough RBCs, ↑ RI, making plenty of RBCs, loosing them too fast ↓ erythrocyte production (↓Reticulocyte Index) [MCV=80-100] bone marrow problem; causes: EPO
deficiency- (2nd to renal failure), can give exogenous EPO; myelofibrosis- bone marrow replaced with scar tissue; aplastic anemia- bone marrow replaced w/ fat
(w/ pancytopenia- deficient in all blood cells) ↑erythrocyte turnover (↑Reticulocyte Index) [MCV=80-100]; causes: hemolytic anemia- breaking down RBCs,
retaining iron; hemorrhagic anemia- menses, ulcers, & colon cancer, can lead to iron deficiency, give iron supplement; sickle cell anemia- cella have ↓life span, faster turnover Other:
diagnosed by appearance of RBCs; causes: spherocytosis, polycythemia- ↑RBCs, thick blood, leads to heart failure RETICULOCYTE INDEX how much reticulocyte count expected to go up in
particular anemia; should be between 1% - 2% in anemics, 0.5-1.5% in non-anemics, anemia will ↑ reticulocyte count; RI= reticulocyte count * ((hematocrit / normal hematocrit [45%]) / #
days as reticulocyte) SERUM IRON & TIBC total iron binding capacity, ↓ hematocrit  need iron in bone marrow available to put in hemoglobin, excess iron stored in liver; ↓ iron in blood not
necessarily iron deficiency anemia- most iron in hemoglobin or bound to transferrin; transferrin: protein carries iron in blood; if iron and transferrin low  anemia of chronic disease; if normal
iron and ↑ transferrin but ↑ t saturation, liver making too much transferrin MEGALOBLASTS OF PERNICOUS ANEMIA B12 & folate deficiency- impair RNA/DNA synthesis, RBCs much bigger than
norm; ↓IF  B12 deficiency  impaired RNA synthesis (Gastric parietal cells secrete IF – deficiency may be genetic or acquired), B12 → neuro symptoms megaloblasts: large, immature nuclei,
finely reticulated chromatin, abundant basophilic cytoplasm; bone marrow aspirate: dispersed nuclear chromatin HYPOCHROMIC MICROCYCTIC ANEMIA OF IRON DEFICIENCY: hypochromic: lots
of pale cells, some dark ones due to blood transfusion, occurs if cannot make enough hemoglobin; could be iron deficiency, would give iron; EPO ↑, producing lots of RBCS but not enough
hemoglobin IRON CYCLE in blood ~100 days; RBCs created in bone marrow→ RBCs broken down in spleen → iron removed from heme (amino acids recycled - remaining to bilirubin)→ iron
attaches to transferrin & reused for production of new RBCs→either stored in liver or goes to bone marrow for use; only get rid of iron by bleeding ROLE OF EPO ↓arterial O2→EPO production→RBC
production→ ↑RBCs→ correction of hypoxia→ normal O2 levels→ kidney stop EPO (- feedback) APLASTIC ANEMIA marked reduction in hematopoitic cells w/ expansion of fat cells usually caused
by toxic chemicals that kill bone marrow, pancytopenia: deficiency in all blood cells SICKLE CELL ANEMIA risk for obstruction of capillaries, if gets stuck→clot  lose bf  pain and tissue destruction
SICKLE CELL HEMOGLOBIN stacked hemoglobin b/c 1 base pair changes confirmation of protein w/ low O2 →spike-shaped cells; sickle cell trait- 1 mutated gene; sickle cell disease- 2 mutated
genes SICKLING OF ERYTHROCYTES HbA: norm adult hemoglobin; HbF: fetal hemoglobin; HbS: sickle cell hemoglobin; ↑sickling on venous side bc naturally ↓O2; cells usually normal size but sickle
w/ ↓ O2 content, pH, temp, plasma vol → ↑sickling bc ↑ hypoxemia → either worsening of symptoms or improvement w/ treatment of O2 and fluis; clinical manifestation: autosplenectomy- spleen
gets progressively smaller, almost all organs effected by ischemia β-THALASSEMIA need 2 α & 2 β to make hemoglobin, genetic mutation  either globin not made in sufficient numbers; making
bad β→ ↑ good α  α aggregates  sticks to RBCs, shortens life because cannot pass through spleen  good cells die quickly  anemia; β more common in US than α, comes from
Mediterranean; transfusion- short term beneficial but long term detrimental (iron overload), phlebotomy doesn’t help bc become anemic again; thalassemia mutation protects against malaria: cell
turnover faster→clear anemia faster, 1 mutation- no anemia or malaria, 2 mutations- anemia & no malaria, no mutations- malaria & no anemia SPHEROCYTOSIS defect cytoskeleton holds
membrane, RBC break off- loss of surface area, harder to get O2 into cells, lose central pallor→ spherical shape→ anemia bc cells don’t live long GLUCOSE-6-PHOSPHATE DEHYDROGENASE
deficiency leads to oxidative damage, 2nd most common genetic mutation, X-linked; macrophages in spleen eat part of cell because it lacks enzyme that helps with oxidative damage, protein
aggregates and splenic macrophage tries to remove aggregates; protects against malaria MICROANGIOPATHIC HEMOLYTIC ANEMIA get stuck in fibrin mesh from clots (DIC) & get sliced, in
kidneys hemoglobin gets stuck in glomerulus & cause damage→ hemolytic uremic syndrome (↑BUN, fragments stuck in glomerulus  acute renal failure), usually see with hemorrhagic E. coli
MYELOFIBROSIS tear shaped RBCs, bone marrow →scar tissue → squeeze RBCs trying to form; extramedullary hematopoiesis (outside of bone marrow) HEMOLYTIC DISEASE OF NEWBORN mom
exposed to rh antigen when giving birth to Rh + baby→ builds rh antibodies→ subsequent pregnancy w/ rh+ baby→ IgG memory cells activate & cross barrier→ antibodies attack baby’s blood
cells→ fetus’s immune cells destroy blood cells→ anemia & large bilirubin load  jaundice TARGET CELLS cells stiffer, normally destroyed in spleen but splenectomy → ↑old cells, cytoskeleton
holding together HOWELL-JOLLY BODIES fragments of DNA left behind by macrophages, seen w/ spenectomy HEMATOPOIETIC CELLS RBCs & megakaryocytes =myeloid cells; mononuclear
phagocytic system: monocyte, macrophage (Kupffer cell-liver, microglia-brain, osteoclast-bone, multinuclear giant cell), dendritic cell (Langerhans cell – skin) ALTERNATIONS OF LEUKOCYTES too
many: - cytosis or – philia too few: - penia shift-to-left: ↑immature cells end up in blood; anemia: erythrocytes coming out earlier CANCER OF HEMATOPOIETIC CELLS cancer at any point along
differentiation of hematopoietic cells, acute toward the top, chronic toward bottom closer to mature cells; leukemia can involve myeloid or lymphoid cells, be acute or chronic; acute lymphocytic
leukemia (ALL): B&T cells; acute myelongenous leukemia (AML): granulocytes, megakaryocytes, erythrocytes; chronic lymphocytic leukemia (CLL): B cells Chromic myelongenous leukemia
(CML): granulocytes, megakaryocytes, erythrocytes myeloma: plasma cells Hodgkin lymphoma: B cells in lymph nodes Non-Hodgkin lymphoma: B & T cells in lymph nodes CELL-SPECIFIC
LEUKEMIAS Cancer in lymphoid branch: lymphocytic cancer; Acute: earlier in development  immature cells Chronic: closer to end product mature cells, Multiple myeloma: cancer of plasma
cells, Acute erythro leukemia: cancer of erythroid stem cell; end up w/ proerythroblasts in blood, Megakaryocyte: ↑ platelet count  problem = clotting, Cancerous Normoblast: pushes out fully
functioning RBCs polycythemia hematocrit 70-80 (dangerously ↑), polycythemia vera: erythrocyte leukemia, moved under erythroid stem cell LEUKEMIA CLINICAL MANIFESTATIONS too much of
one cell leads to not enough of another; anemia: bone marrow not producing RBCs; bleeding: not making platelets; DIC: not enough megakaryocytes (2nd to something); infection: not enough
good immune cells; bone pain: all happening in bone marrow; ↑uric acid: waste product from processing nucleotides when destroying cells; liver spleen & lymph node enlargement; weight ↓: loss
of appetite and calories ACUTE LEUKEMIA more serious than chronic, rapid ↑ in immature blood cells, rapid progression of malignant cells, ↓production of norm blood cells, associated w/ radiation
exposure, more common in kids, ↓survival in adults ALL: 80% of childhood leukemias, 90% survival, mostly B-cell precursors, associated w/ Philadelphia chromosome (translocation between chr
9&22); AML: most deadly, 1% of cancer deaths, wide age range, aduLsurvival 20%, 8 subtypes (M0-M7 cover all myeloid pathways) CHRONIC LEUKEMIAS buildup of relatively mature blood cells,
progresses slowly, abnormal cells in blood CLL: B cells, hypogammaglobulinemia (dt immature B cells or not useful B cellsinfection), affects elderly, good survival CML: young adults, immature
neutrophils are being oushed out, Philadelphia chrom, poor survival MULTIPLE MYELOMA cancer from plasma cell- making tons of antibody in bone marrow even though infection cleared clinical
presentation: hypergammaglobulinemia (useless against everything other than 1 antigen), displace other bone marrow cells as well as plasma cells, bone pain from punched out lesions, ↑ serum
antibody levels, infection, ↓serum albumin concentration- liver doesn’t produce albumin bc of ↑antibodies in blood, protein in urine - Bence-Jones proteins (loose Ig light chains glomerular
damagerenal failure) LYMPHADENOPATHY neck, axillary, & groin – swelling of lymph nodes (lymphoma) HODGKINS LYMPHOMA B cell neoplasm spreads from 1 lymph node to next, ReedSternberg cells, good survival rate, 5 sub-types NON-HODGKIN LYMPHOMA over 30 types, swelling of lymph nodes not Hodgkin lymphoma CORONAL SECTION gray matter: along cortex, neuronal
cell bodies, computation white matter: middle brain, myelinated axons carrying info, connection; convolutions: allow for more gray matter GENERAL ANATOMY longitudinal fissure: splits brain into
right/left cingulate gyrus: anatomical landmark corpus callosum: allows R & L sides to communicate septum: between L & R lateral ventricles caudate nucleus (along w/ globus pallidus &
putamen): form striatum – caudate & globus pallidus part of basal ganglia, globus pallidus & putamen form lenticular nucleus insula: big convolution↑ surface area – sylvian fissure forms insula
anterior commissure: communicate L to R amygdaloidal nucleus: almond shape, fear center hippocampus: memory center, near amygdala internal capsule: all info coming & going passesdamage=bad corona radiate: fibers span out NEURONS pseudounipolar cells: sensory nerves, cell body long dendrite & axon, nerve in finger-dendrite up to dorsal root ganglia to spinal cord
&immediately to brain multipolar cells: majority of neurons, lots of dendrites, at axon terminus Ca comes in releases neurotransmitter binds on postsynaptic cleft hyperpolarization or
depolarization bipolar neurons: in eyes & ears myelinated: signal travels fastest rate (bigger = faster), Schwann cell- PNS, oligodendrocyte-CNS GLIAL CELLS Astrocyte: wraps capillary, nothing
leaves capillary w/o going through astrocyte (blood brain barrier) oligodendrocytes: myelate axons in CNS Microglial cells: macrophage ependymal cells: line ventricles & ducts for CSF, cilia to
move CSF, choroid plexus- create CSF PARTS OF BRAIN central sulcus- in front is precentral gyrus & behind is postcentral gyrus, lateral fissure- separates frontal & temporal lobes brodmann’s area:
gray matter of cerebral cortex has 6 layers of cell types – way of numbering these FRONT OF BRAIN what you do to the world precentral gyrus: neurons of upper neuron→ muscle fiber contract,
primary somatic motor areas premotor cortex: coordinate muscles, frontal eye field- converge & focus, Broca’s area- coordinating muscles of speech prefrontal area: personality, make plans,
store declarative memories BACK OF BRAIN postcentral gyrus: sensing an individual sensory nerve ending, primary somatic sensory cortex visual cortex: approximately each pixel (rod or cone) has
neuron auditory cortex: decode sound, frequency decomposition association areas: putting things together, somatic sensory, visual, & auditory association areas angular gyrus: where we store
information about nouns, close to key language center- Wernicke’s area HOMONCULUS describing sensory cortex in visual way, we don’t have equitable distribution of motor or sensory neurons
across body CORTICOSPINAL TRACT most important motor tract, starts in cortex & goes to spine, do not control head, face, larynx, & pharynx upper motor neuron: starts in motor cortex lower motor
neuron: starts in spinal cord; 80-90% cross in medulla, rest decussate in anterior white commissure of spinal cord CORTICOBULBAR TRACT innervate cranial nerves; upper motor neurons of lower
neurons of cranial nerves that control skeletal muscles; cranial nerves 3,4,6: ocular muscles 5: trigeminal- facial senses & mastication muscles 7: facial- facial expressions 9: glossopharyngealswallowing 10: vagus- many functions, skeletal muscles of pharynx & palate 11: accessory- sternocleidomastoid & trapezius 12: hypoglossal- tongue muscles, 1, 2, and 8= only that do not have
motor components CRANIAL NERVES 1-olfactoy 2- optic 3-oculomotor 4- trochlear 5- trigeminal 6- abducent 7- facial 8- vestibulocochlear 9- glossopharyngeal 10- vagus 11- accessory 12hypoglossal RUBROSPINAL & RETICULOSPINAL TRACTS modulate action of muscles; Parkinson’s- damage to substantia nigra normal strength but trouble initating action  resting tremors MAJOR
SENSORY PATHWAYS Dorsal Column Medial Leminiscus: travel up dorsal columns of spinal cordcross at medulla  medial lemniscus thalamus  prim sensory nucleus, cell bodies in dorsal root
ganglia; fine touch & kinesthesis Spinothalamic: spinal cord to thalamus, pain & temp, immediate cross over in spinal cord thalamusprim sensory cortex; cell bodies in dorsal root ganglia PAIN
SYNAPSES pain synapses & crosses at spinal cord; large fiber impulses block pain & small fiber impulses ↑pain; by rubbing when it hurts activate larger fiber impulses to block pain; brain
modulates sensitivity of pathways REFERRED PAIN pain in R side & R shoulder w/ running- liver complaining heart: radiating down L arm to neck kidney: back & flanks SPINAL CORD 7 cervical
vertebrae (8 cervical nerves), 12 thoracic, 5 lumbar, 5 sacral; dura mater (outer), arachnoid, & pia mater SOMATIC MOTOR NEURONS upper motor neuron synapses w/ lower motor neuron, lower
motor neuron runs to neuromuscular junction to innervate muscle SENSORY NEURONS nerve ending, long dendrite, cell body & dorsal root ganglion, axon enter spinal cord via dorsal horn
AUTONOMIC MOTOR NEURONS axon out of spinal cord, 1 synapse, postsynaptic neuron innervates end organ; dorsal (posterior): sensory ventral (anterior): motor SOMATIC MOTOR NEURONS spinal
cord has lower motor neuron that runs to skeletal muscle, nothing between except axon AUTONOMIC MOTOR NEURON one synapse between spinal cord and end organ; AUTONOMIC NERVOUS
SYSTEM 1st axons neurotransmitter is acetylcholine sympathetic: T1-L2/3, none on cranial nerves, 2nd neurotransmitter norepinephrine parasympathetic: cranial nerves 3, 7, 9, 10 & sacral S2-S4;
vagus nerve controls below head & above descending colon, sacral parasympathetics control distal colon, bladder, & genitals BLOOD SUPPLY TO BRAIN & HEAD brachiocephalic: R side, R common
carotid, R subclavian; L common carotid & L subclavian come off aorta common carotid: split to internal & external carotid, vertebral arteries come off L & R subclavians CIRCLE OF WILLIS 3 ways of
getting blood to brain; anterior, middle, & posterior cerebral arteries (anterior & posterior communicating arteries) BLOOD TO BRAIN anterior cerebral: medial frontal & medial parietal middle
cerebral: lateral sections posterior cerebral: occipital & lower temporal lobes VENTRICLES & CSF lateral, 3rd, & 4th ventricles CSF flow: lateral3rd cerebral aqueduct4th 2 lateral foramina & 1
medial foramen; circulates through brain in arachnoid region, reabsorbed by arachnoid granulation & dumped into superior sagittal sinus; 150mL in body at a time, make 500mL per day, replace
3x per day MENINGES dura matter: tough leathery coating, adherent to skull; Arachnoid mater: thin layer spider web like, CSF circulates through here; Pia mater: layer closest to brain- adheres to
brain TYPE OF STROKES if neurons die, gone for good, need to correct problems as fast as possible to prevent additional damage ischemic: 80%, blood flow cut off, atherosclerotic plaque ruptures 
embolism  tissue factor  blood flow cut off  cells die; give fibrinolytic drug hemorrhagic: bleeding in brain, ↑ pressure, herniation through foramen magnum, vessels feeding basal ganglia like
to rupture – if progresses to internal capsule=bad; do not give fibrinolytic drug determining type: CT scan to look for presence of blood, time = damage LOCATION OF STROKE can occur anywhere
in CNS; many strokes happen in middle cerebral arterylanguage deficits; symptoms correlate with the affected part of the brain Circle of Willis: carotids come in here, anterior cerebral feeds
medial part of brain, middle feeds lateral part of brain, posterior feeds posterior part of cerebrum frontal & temporal lobe strokes-survivable, lose memories but can make more internal capsule:
communication between cerebrum and body affected  paralysis or neuropathy brainstem strokes- devastating middle cerebral arteries: popular  language deficits; blood vessels feeding
basal ganglia- common for hemorrhagic stroke LANGUAGE DEFICITS middle cerebral arteries: popular  language deficits; if R handedlanguage only on L side, if R handed could have
language on L, R, or both; if on both sides, stroke on either  language deficits Dysphasia: bad language; Broca’s area: can’t control muscles of speech, understand language but cannot generate
it Wernicke’s area: can speak coherently but its meaningless Global: frontotemporal, all language impaired or lost Anomia: angular gyrus/posterior superior temporal- inability to name objects
Transcortical motor: anterior presylvian fissure- impaired output transcortical sensory: posterior presylvian fissure- impaired input w/ impaired output dysarthria: difficulty speaking but language is
clear- motor prob dyslexia: difficulty reading alexia: can’t read dysgraphia: difficulty writing agraphia: can’t write ANEURISMS chance of them rupturing, sub-arachnoid hematoma, typically on
circle of Willis clinical sign: severe & sudden headache w/ eventual loss of CNS function CRANIAL BLEEDS ↑ pressure w/ poor circulation, brain continues to ↑ pressure, drill hole to let it out AV
MALFORMATIONS particular risk for rupturing get hemorrhagic stroke; arteriovenous anastomosis: blood goes from arterial side to venous side w/o going through capillary, lots of blood, may
rupture; hard to detect, CT scan to detect, similar clinical signs as ruptured aneurism but parenchymal bleed- not SAH treatment: clip off AVM anastomosis HERNIATION don’t want to pull out brain
through foramen magnum, lumbar puncture- if draw out too much CSF  brain will suck out, if something is causing ↑intracranial pressurepushing brain through foramen magnum more likely, 1st
medulla oblongata goes through- loss of consciousness; 3 types of herniations: subfalcine- brain pushed under falx cerebri; uncinate- herniation of temporal lobe into tentorial notch; tonsillardownward displacement of brain stem through tentorial notch HIGH PRESSURE HYDROCEPHALUS CSF in brain, occurs slowly clinical signs: heachaches w/ nausea & vomiting, mental deficits,
seizures, LOC noncommunicating hydrocephalus: ↑ pressure, ventricles can’t communicate w/ drainage, usually caused by obstruction of outflow, ventricles get bigger & bigger as fluid builds up,
treatment to stick a shunt to release fluid, common in babies & children- expansion of skull in children Communicating: ↑ pressure, CSF can flow but ventricles enlarge, ↓ uptake of CSF by
arachnoid granulations, more common in adults NORMAL PRESSURE HYDROCEPHALUS brain atrophies, ventrivles get bigger secondary to cortex getting smaller, chronic intermittent high pressure;
ex vacuo: atrophy of brain; common reason in children- ventricle drainage blocked, no lymph nodes; symptoms: hedache, difficulty functioning TRAUMA & HEMATOMAS whack someone in head
 can get intracranial bleed; middle meningeal artery rupture: epidural hematoma (outside of dura mater) damage to bridging veins: subdural hematoma Treatment- drill hole, blood squirts out &
pressure released; chronic subdural- lump on person’s head ruptured aneurysm: subarachnoid hematoma, large artery ruptures  aneurysm  bleeds into subarachnoid space hemorrhagic
stroke: parenchymal bleed traumatic brain injury: damage to brain, moves forward & backward  damage to both ends spinal cord trauma: vertebral fractures may damage spinal cord, damage
doesn’t repair; original damagehemorrhageneutrophils bring inflammatory cytokines ↓ bf to spinal cordfree ironRBC & platelet aggregation; treatment- therapeutic hypothermia,
decreases inflammatory response to prevent further spinal cord damage from secondary response SEVERE AN AXON can’t repair injury site, regrow axon- make protein in cell body & send it down
axonmove 4mm/day; if axonal tract clear & Schwann cells presentaxon finds target; less mylenated, less likely to recover DEGENERATIVE DISK DISEASE nucleus pulposus- squishy stiff in vertebral
column, annulus fibrosus- fibrocartilage in vertebral column, herniation of posterior side can interfere w/ spinal nerve; whatever it impacts (motor/sensory) will be impaired; can have pain w/o
spinal stenosis CANCER many= metastases, can’t get cancer of neurons; neuroblastoma: cancer of neuro-precursor cell, common in childrens gliomas: involves glial cells which replicate; mean
survival= 5 yrs, can be in spinal cord; astrocytoma- grade IV= very poor survival; glioblastoma- most common brain cancer- poorly differentiated neoplastic astrocytes, poor survival rate;
oligodendroglioma; ependymoma- line ventricles microglial cells don’t cause cancer; medulloblastoma, meningioma, schwannoma, metastatic (spread from another body part); clinical
presentation: persistent headache dt ↑ pressure, cerebral edema, vomiting & seizures, papilledema- brain pushing against eyes & optic disc compressed (look into eyes to see this), lose muscle
strength & coordination INTRACRANIAL TUMORS Neoplasm increases pressure and compression  headaches, vomiting, seizures  diminished cognitive function resulting in behavior malfunction
over time; Schwanoma: found in PNS 8th cranial nerve schwannoma, “acoustic neuroma” presentation: headaches, compression of cerebral aqueduct, mental deficits,
seizure, damaged hearing & vestibular system of that side- balance probs; easier to cut out, good prognosis SPINAL TUMORS meningioma: cancer of cells that form
meninges, not hard to cut out INTRACRANIAL INFECTION bacterial infections uncommon, damage to axons or cell bodies causes irreversible damage meningitis: CSF
cloudy, ↑leukocytes, ↓glucose (bacterial cells are using it) VIRAL INFECTION virus doesn’t want to kill host; rabies and herpes= exceptions PRION infectious agent is precursor
protein in CNS, protein changes shape & ones around it also change; miss-folds  becomes round  causes good proteins to also miss-fold and become misshapen over
time  aggregates; slow virus MAD COW DISEASE Bovine spongiform encephalopathy, rare in humans, only from CNS material, must be introduced into bloodstream via
sores in mouth (kids losing teeth), 200 cases, 100% fatal Papa New Guinea: cannibalism funeral rites- Kuru Creutzfeldt- Jacob Disease: inherited form- prion precursor
more likely to misfold, spontaneous, older patients DEGENERATION Alzheimer’s, Parkinson’s, Huntington’s, Poliomyelitis, Amyotrophic lateral sclerosis, MS, Guillain- Barre,
Myasthenia gravis ALZHEIMER’S DISEASE pre-senile dementia; frontal lobe atrophy, wide sulci & thin gyri, both anterior(past) & retro(making new) grade amnesia, only
diagnosed after death amyloid precursor protein: if not chopped properly Aβ aggregates form→amyloid fibrils  death of neurons in frontal lobe  loss of function
genetic component: some people clear protein, ↑ w/ DM2 UPPER MOTOR NEURONS cell body in primary motor cortex, axon runs down spinal cord & synapses w/ lower
motor neuron then muscle Damage: birth injuries, neoplasms, trauma, inflammation, amyotrophic lateral sclerosis, vascular lesions (CVA, thrombosis, embolism, hemorrhage, aneurysms),
demyelinating, degenerative diseases- multiple sclerosis LOWER MOTOR NEURONS polio- muscle weakness and paralysis; amyotrophic lateral sclerosis (ALS); demyelinating (Guillain-Barre); probs
w/ muscle junction- myasthenia gravis, damage to muscle – muscular dystrophy PARKINSON’S affects motor skills but minimal affect on thought processes; L-DOPA helps tremors & trance state
Substantia nigra: filled w/ neuromelanin byproduct of dopamine, not present w/ Parkinson’s Lewy body: protein aggregate in damaged neurons, lose dopamine going to basal ganglia Basal
ganglia: inhibitory neurons, start & stop actions presentation: resting tremor but smooth movement, once person starts moving do not need basal ganglia until they need to stop;
dysdiadochokinesis- trouble w/ RAMs, unsteady gait, shuffling, no facial expressions, trouble coughing & swallowing (kills eventually), late progression- dementia, SNS probs HUNTINGTON’s CHOREA
overactive initiation of movement → jerky motions; basal ganglia damage looks like hydrocephalus bc atrophy of caudate & putamen; trinucleotide repeat CAG- autosomal dominant, every
generation starts getting HD earlier bc ↑copies TARDIVE DYSKINESIA dopamine supersensitivity – result of psychiatric/antipsychotic meds, high dose or long time→ version of chorea, irreversible
MULTIPLE SCLEROSIS immune system attacks myelin of CNS (white matter)- kills oligodendrocytes; axon w/o myelin won’t work; motor, sensory, cognitive probs; myelin can regrow, (attacks &
remission) 4 types: relapsing remitting- where most people start, get worse then get better; progressive relapsing- worse after attacks; primary progressing- steadily worse w/o attacks; secondary
progressing- relapsing remitting  primary progressing DENERVATION & RE-INNERVATION happens w/ polio, lose lower motor neuron & muscle innervation bc of virus→ profound weakness, resp
probs, eventually paralysis recover: denervated muscle fibers connect to surviving lower motor neurons, norm strength but worse fine motor control, weaker faster w/ age post-polio syndrome: had
it as kids, half have PPS later in life normal motor units: 2 adjacent motor units shown segmental demyelination: random internodes of myelin injured & remyelinated by Schwann cells, axon &
myocytes intact axonal degeneration: axon & myelin sheath undergo anterograde degeneration, denervation atrophy of myocytes DEMYELINATION OF PNS Guillain- Barre, Schwann cells
remyelinate axons, immune attacks it, Schwann remyelinates  rings, immune system ultimately wins GI ORGANS primary: oral cavity, esophagus, stomach, small intestine (duodenum, jejunum,
ileum), large intestine (cecum, ascending colon, transverse colon, descending colon, sigmoid colon) secondary: gallbladder, pancreas, liver SITES OF ABSORPTION stomach: H2O, alcohol
duodenum: iron, Ca, fats, H2O, sugars, protein, vitamins, Mg, Na Jejunum: sugars, protein Ileum: bile salts, B12, Cl Colon: H2O, electrolytes STOMACH PHYSIOLOGY isotonic slurry, IF secreted to bind
B12 (attaches to transcobalamin), later absorbed in ileum acidity: pH 2 (kills most microbes & denatures proteins), CO2+H2O→ H+ + HCO3- , bicarb dumped into blood→pancreas &
gallbladder→duodenum ↑ chyme pH, H+ goes to blood to neutralize bicarb from stomach, if vomit after acidic production→alkaline proteases: cannot contact cells of lining, keep cells away from
acidic environment (deep gastric pits & covered by mucosal layers) PHYSIOLOGY OF INTESTINES small intestine general: contents called chyme, ↑pH to 8 w/ bicarb in duodenum, pyloric sphincter
between stomach & duodenum (paces chyme coming into duodenum), have villi to ↑SA (lacteal drains lymph), 3 days for new cell to reach top, replace 2x/wk, duodenum: 10 in, pancreatic duct
joins common bile duct (from liver & gallbladder) at ampulla of Vater (sphincter of Oddi allows contents to enter duodenum- contains bicarb, biliary secretions, & pancreatic digestive enzymes)
jejunum: 20 ft, bulk of absorption Ileum: 6 ft, absorb B12 and bile salts from liver, bile salts emulsify fats (recycled back to liver) Ileocecal sphincter: between ileum and cecum Colon: reabsorb
bicarb; chronic diarrhea → acidosis wall of intestines: innermost- single columnar epithelial (absorb nutrients), lamina propria, musclaris mucosa (move mucus to ↑contact between epithelium &
contents for absorption), submucosa (glands), submucosal plexus (innervates submucosa & mucosa, muscularis mucosa and
glandular tissue), lymph nodes (lots of lymphatic tissue in GI tract), muscularis (circular & longitudinal layers), myenteric plexus
(between circular & longitudinal- innervates muscularis & responsible for peristalsis), serosa, mesentary; GI is largest lymphatic
organ peristalsis: stomach noises 2-3 hrs after eating, big wave starts in stomach→cecum, clears out intestine & happens 1x/hr,
2-4 hrs from mouth→ cecum (20 hrs from cecum to anus) ESOPHAGEAL DISORDERS- HIATAL HERNIA stomach goes through
esophageal hiatus above diaphragm into supradiaphragmatic area, ↑incidence w/ age symptoms: heartburn & regurgitation,
pouch above stomach irritates the lining of the diaphragm; 95% sliding hernia ACHALASIA lower esophageal sphincter doesn’t
open properly→stuff sits in lower esophagus loss of intrinsic inhibitory innervation of LES: aperistalis, incomplete relaxation of LES, ↑
resting tone of LES problems: dysphagia (painful swallow), mucosal inflammation & ulceration (espophagus not made to have
bolus sitting there), squamous cell carcinoma (5%) ESOPHAGEAL VARICES liver problems: hepatic portal HTN 3 ways blood
escapes hepatic portal system: rectum, lower esophagus, around umbilicus (↑flow through capillary beds in LE→ varicose veins)
cause: impaired hepatic portal bf associated w/ alcoholic cirrhosis (2/3 cirrhosis patients)  ↑ blood flow through capillary beds
in LE  varicose veins problem: rupture→ hematemesis (20-30% die on episode, 70% recurrence) treatment: balloon that stops
bleeding, 70% recurrence GERD (reflux esophagitis) LE doesn’t close tightly enough- not chemically strong→ gastric juices splash up and irritate LE  chronic heart burn contributing causes:
obesity, hiatal hernia, vagal nerve abnormalities (not closing sphincter properly) problems: heartburn, Barrett esophagus BARRETT’S ESOPHAGUS replacement of norm stratified squamous mucosa
w/ metaplastic columnar epithelium w/ goblet cells, allow LE to withstand exposure to acid cause: long-standing GERD problem: adenocarcinoma (w/ heartburn) ESOPHAGEAL CANCER squamous
cell carcinoma: tobacco/alcohol, achalasia, very hot tea (>65C); higher in esophagus; first sign= dysphagia, tumor forms band around esophagus preventing normal movement of bolus, seems
like achalasia adenocarcinoma: (more common in US) Barret esophagus symptoms: dysphagia & obstruction (typically late in cancer progression) CHRONIC GASTRTIS & PEPTIC ULCERATION
chronic gastritis: H Pylori (bacteria) causes chronic mucosal inflammation, usually asymptomatic until acid progresses CG problems: upper abdominal discomfort, nausea & vomiting, ulcersChronic gastritis→ peptic ulcers Peptic ulcers: mucosal lining of stomach is eroded causing pain  chronic lesions, gastric contents chewing away at muscularis mucosae anywhere GI tract is
exposed to acid-peptic juices anywhere in GI, 98% duodenum & stomach, H pyloric present in 70-90% duodenal & 70% gastric, 60% of population has H Pylori, 10-20% ppl w/ H pylori get ulcers
aggravating peptic ulcer causes: NSAIDs, smoking, alcohol, corticosteroids, stress personality peptic ulcer problems: epigastric pain, nausea & vomiting, hemorrhage & perforation (become
hypotensive→acute tubular necrosis  RF), not progress to cancer, impair quality of life not shorten it ACUTE GASTRITIS acute mucosal inflammation, usually transient causes: heavy NSAID use
(inhibit production of prostaglandins which signals mucosal layer to be produced), excessive alcohol use, heavy smoking, cancer chemo, uremia, systemic infections, severe stress (trauma, burns,
surgery), ischemia & shock, ingestion of caustic agents, mechanical trauma (NG intubation) problems: epigastric pain w/ nausea, vomiting, hematemesis & melena ACUTE GASTRIC (stress) ULCERS
focal, acute gastric mucosal defects resulting from severe stress, 2nd to another problem- treat underlying prob causes: severe trauma, extensive burns,
trauma to CNS or intracerebral bleed, gastric irritants (NSAIDs); treat primary problem and stomach will heal STOMACH CANCER rare incidence of
intestinal-type adenocarcinoma dt refrigeration, carcinoma 90%, gastric carcinoma 2nd leading cause of death worldwide causes for intestinal-type
adenocarcinoma: nitrites/ nitrates preservative for meat, smoked food, pickled food, excessive salt, ↓ by fruit & veggie consumption, chronic gastritis, H
pylori infection diffuse carcinoma: not ↓ in frequency, not as prominent to begin with, risk factors poorly understood, H pylori absent DIGESTION &
ABSORPTION starch: in mouth salivary amylase→dextrins, oligosaccharides→ pancreatic amylase → lactose, maltose, sucrose→brush-border enzymes
in small intestine (lactase, maltase, sucrase) → galactose, glucose, fructose→ absorbed by capillaries in villa & transported to liver by portal vein;
glucose transported w/ Na coupled receptors (active), fructose & galactose passive transport (15% of our cals from fructose→ hyperglycemic probs not
on blood glucose test) protein: pepsin in HCl in stomach (proteases come from pancreas & do not become active until they leave it, denatures
protein)→proteoses, peptones→ pancreatic enzymes in small intestine→small polypeptides, dipeptides→ brush-border enzymes in small intestine→amino acids→
absorbed by capillaries in villa & transported to liver by hepatic portal vein fats: unemulsified fats→ emulsifying agents in small intestine (bile acids, fatty acids,
mono-glycerides, lecithin, cholesterol, protein) & pancreatic lipases in small intestine → monoglycerides & fatty acids (→absorbed by lacteals in villi & transported
to liver in systemic circulation) or glycerol & fatty acids (→ absorbed by capillaries in villi & transported to lover by portal vain; glucose and sodium transport:
isotonic slurry- Na+ and water ~same concentration as the blood, Na+ wants to move into the cell where ATPases pump Na+ into the villi; glucose brought into the
cell via active transport, fructose via passive transport with water; majority of carbs = glucose brought in by coupled receptor BLOOD SUPPLY FOR INTESTINES
superior mesenteric artery feeds most of small & large intestine up to splenic flexure; inferior mesenteric artery feeds from splenic flexure to rectum; splenic flexure
has weak blood supply- dangerous spot for ischemia HIRSCHSPRUNG (congenital megacolon) caudal migration of neural crest cells fails to reach anus leaving aganglionic segment of distal colon
lacking myenteric plexuses→ no peristalsis or bms→ fecal matter collects problems: obstruction, enterocolitis, perforation; colon will get bigger as fecal matter collects  perforation and sepsis;
treatment: removing aganglionic segment (small section- not a problem; big section- chronic diarrhea & impaired bicarb & Na reabsorption) ISCHEMIC BOWEL DISEASE acute occlusion or
hypoperfusion can lead to infarction; mucosal- not serious bc replace layer often, mural- entire mucosal layer, transmural- across wall, friable material easily ruptures→fecal leak to
abdomen→sepsis causes: any kind of hypotensive shock; arterial thrombosis, arterial embolism, venous thrombosis, nonocclusive ischemia (cardiac failure, shock, dehydration, vasoconstrictive
drugs), mechanical obstruction (volvulus, stricture, herniation); mortality rate for transmural about 99% HEMORRHOIDS persistently ↑ venous pressure in hemorrhoidal plexus causes variceal
dilations/dilated veins causes: straining during defecation, pregnancy, hepatic portal htn DIARRHEA absorb water from food during digestion, if moves too fast  watery stool; secretory: vibrio
cholera (Cholera)- causes epithelial cells to secrete Cl into small intestine →impedes Na absorption→ can’t absorb H2O; voluminous watery diarrhea, contaminated H2O supply, spreads quickly
and difficult to eliminate, results in death by dehydration Osmotic: gut lavage (Golytely), overwhelms GI tract w/ polyethylene glycol→holds H2O in GI tract (acts as osmotic diuretic)→ clears colon
Exudative: destruction of epithelial layer, dead cells in lumen act as osmotic agents (Shigella, Salmonella, Campylobacter) Malabsorption: can’t absorb lactose by itself, but bacteria in colon can
and they replicate rapidly (giardia, lymphatic obstruction, defective absorption) happens w/ lactose intolerance→bacteria feed on lactose; common, gas, bloating, diarrhea Hyperthyroidism:
deranged motility, GI tract hypermobile, not enough time to reabsorb H2O INFLAMMATORY BOWEL DISEASE Crohn’s disease: skip lesions & good tissue, anywhere from mouth to anus, transmural
inflammation- long deep fissures, fistulas from lumen of intestine to abdomen (improper connection) Ulcerative colitis: inflammation of colon starts at rectum, continuous section of colon that is
involved; tissue in colon being eroded, starts at rectum & continues, pseudopolyps (tissue around it has been eroded & part of it sticks out to look like a polyp) Symptoms in common: diarrhea, loss
of appetite, painful bms, frequent bms, wt loss, fatigue HOOKWORM hook onto intestines & suck blood→hemorrhagic anemia with no blood coming out; turns off immune system & alleviates some
of symptoms & probs associated w/ Crohn’s & asthma DIVERTICULOSIS/ DIVERTICULITIS diverticula are pouches protruding out of bowel, 50% of ppl >50 yrs old, worse in lower left quad where stool is
more solid problems: lower left quad discomfort, bleeding, perforation, fistula formation (following perforation), fecal matter leakage; treatment: ↑fiber BOWEL OBSTRUCTION chyme can’t move
through the lumen properly mechanical obstructions: hernias (intestine seeps through inguinal canal- hard to move things through, blood has a hard time nourishing  ischemic damage),
adhesions (post abd surgery, scar tissue bind 2 parts of bowel), intussusception (in kids, 1 piece slides into other, lumen decreased), volvulus (twisting of intestines) Pseudo-obstructions: paralytic
ileus (postoperative), bowel infarction (if muscle damaged→no peristalsis in dead spot), myopathies & neuropathies (Hirschsprung) COLON CANCER large intestine= most common site, small
intestine v rare, ↑w/ age, asymptomatic for years Polyp: tumorous mass protruding into lumen Pedunculated: having a stalk Sessile: not having a stalk Hyperplastic: ↑ # of cells – not cancer Nonneoplastic: not cancerous Neoplastic: abnorm disorganized growth – can be cancer Adenoma: neoplastic polyps arising from epithelial proliferation & dysplasia Adenocarcinoma: cancer arising
from adenomatous polyps (~98% of colorectal cancers) Colorectal Carcinoma: 150,00 cases/year & 50,000 deaths in US, 6% incidence 2% death common symptoms: pain, obstruction, changes in
bowel habit left side symptoms: (descending colon, sigmoid colon, rectum) visible blood in stool, left lower quad discomfort; no anemia because pt will see blood early and get it checked right
side symptoms: (cecum, ascending colon) fatigue, weakness, iron deficient anemia, won’t see blood in stool bc broken down but will see blood on guiac stool test COLON CANCER STAGING Tis:
earliest stage, involves only mucosa T1: cancer grown through muscularis mucosa & extends into submucosa T2: cancer grown through submucosa & extends into muscularis propria (outer muscle
layer) T3: grown through muscularis propria & into subserosa but not to any neighboring organs or tissues T4: grown through wall of colon or rectum & into nearby tissues or organs N0: no lymph
involvement N1: cancer cells found in 1-3 nearby lymph nodes N2: cancer cells found in 4+ nearby lymph nodes M0: no distant spread M1: distant spread present LIVER biggest visceral organ,
blood passes through slowly allowing hepatocytes to detoxify blood HEPATIC PORTAL SYSTEM all blood from abdominal viscera drains though, anything eaten goes straight to liver before rest of
body sees it; liver detoxifies & cleans blood, ¼ CO at rest (20% goes through kidney, 50% of blood is filtered at rest), from LE to rectum, spleen & pancreas drains through hepatic portal circulation
(not kidneys), makes bile which is stored in gallbladder (released into duodenum when we eat), bile= everything coming out of the liver or a specific, narrow class of liver output pancreas:
produces digestive enzymes to be released into duodenum after eating, Sphincter of Oddi controls release LOBULES portal triad 4 parts: hepatic artery (20% of blood entering)- brings in fresh,
oxygenated blood from the aorta; hepatic portal vein (80% of blood entering liver)- deoxygenated blood from GI tract; bile duct- brings bile out of liver; lymphatics (50% of lymph production)-
brings lymph out of liver; blood: mixed blood drains into sinusoids→central vein→ hepatic vein →inferior vena cava, travels slowly to clear toxins; blood moves slowly from hepatic artery and portal
vein to central vein, bile and lymph move in opposite directions back toward the portal triad, bile collects to become bile duct Kupffer cells: macrophages, phagocytose bad material; fat storing
cells store lipid- soluble vitamins reticular fibers: connective tissue over solid organs, give structure; liver not that strong, like big sponge HEPATOCYTE FUNCTION space of Disse where lymph forms,
same protein content as liver blood glucose/protein: stores glucose as glycogen, reduces post-meal hyperglycemia & between-meal hypoglycemia; after meals- take up amino acids, deliver to
hepatocytes for synthesis of plasma proteins & LDL, amino acid reserves in liver (1 day worth) bile: made in liver (bile salts=bile acid), salts emulsify fats (- charge), similar to cholesterol
(amphipathic), released into bile canaliculi (gap between two cells  bile duct  gallbladder  duodenum), ileum reabsorbs bile to be reprocessed and recycled in liver bilirubin: result of broken
down heme, heme = iron & porphyrin ring → biliverdin (green)→bilirubin (yellow-orange), unconjugated bilirubin is lipophilic (can’t get rid of it in the kidney)→ binds to albumin in blood→in liver
hepatocytes attach glucuronic acid→conjugation (becomes H2O soluble)  released into bile canaliculi  dupdenum, gives feces dark color (can make urine dark) FIBROSIS & CIRRHOSIS fibrous
tissue formed w/ inflammation (macrophages activate, stimulating fibroblasts to lay down collagen), bridging fibrosis  link regions of liver continuous fibrosis subdivides liver into nodules of
regenerating hepatocytes surrounded by scar tissue; fibrosis irreversible consequence of hepatic damage→ ↑blood flow resistance, greatly impair blood flow through liver LAB EVALUATION OF
LIVER DISEASE ALT & AST: enzymes within hepatocyte, ↑ if hepatocyte damage/death serum bilirubin: not H2O soluble until conjugated by liver; test for direct/conjugated & total (total – direct =
unconjugated) AP/ALP/ALKP/GGT: biliary tract damage, cells lining bile duct, AP also in bone albumin: if liver failing, not synthesized; ↓ albumin and ↓ total protein  liver damage, if only albumin
may be a kidney problem prothrombin time: measures clotting time, liver makes clotting factors (requires vit. K) & things that break down clots (plasminogen), if liver failing ↑ clotting time but more
clotting also dt ↓ fibrinolytic factors, coagulopathy- prob w/ too much or not enough clotting; ↓clotting factors=bruises serum ammonia: liver deaminates amino acids & joins them to make urea, if
liver damaged ammonia released (can lead to encephalopathy bc ammonia can cross BBB) CONSEQUENCES OF LIVER DISEASE jaundice/cholestasis- turning yellow from bilirubin;
hypoalbuminemia- not making enough albumin; hyperammonemia- liver is not turning ammonia into anemia, hypoglycemia- btwn meals liver controls glucose, if failing  ↓ glucose, fector
hepaticus- toxins in liver find way to lungs→terrible breath; hypogonadism- liver clears steroid hormones- improper clearance of estrogen→ ↓LH & FSH); gynecomastia- buildup of estrogen; obese,
alcoholic males getting breast cancer, fat converts testosterone to estrogen, a failing liver is not clearing estrogen  breast development palmar erythema- red palms- estrogen prob; spider
angiomas- red dilated capillaries dt cap sphincter failure- estrogen prob, wt loss, muscle wasting, depression (psych probs, hepatic encephalopathy) HEPATIC PORTAL HYPERTENSION All blood from
the abdominal organs is draining through the liver with very low pressure; if blood cannot get through liver→ fluid back up → ascites, esophageal varices (bleeding), hemorrhoids, caput medusa,
splenomegaly LIFE THREATENING COMPLICATIONS multiple organ failure: liver dies, takes all other organs with it; coagulopathy: slower to clot and unclot  bleed and clot excessively;
encephalopathy from buildup of ammonia hepatorenal syndrome: if liver stops working, kidneys stop w/in few days usually due to insufficient blood flow, if fix liver, kidneys come right back;
esophageal varices rupture; hepatocellular carcinoma BILIRUBIN METABOLISM AND FAILURE RBCs  get rid of globular protein  heme  biliverdin  bilirubin  binds to albumin, brought back to
the liver  conjugated by glucuronide in hepatocytes dumped into duodenum  deconjugated into urobilinogen half absorbed, converted to urobilin and excreted by kidney (makes urine
yellow), other half in colon converted to stercobilin (brown) and excreted in feces JAUNDICE buildup of bilirubin in blood causes: 1. excess bilirubin production (hemolytic anemia) 2. ↓hepatic
uptake, 3. impaired conjugation, 4. ↓hepatocellular excretion, 5. impaired bile flow causes 1-3: result in unconjugated bilirubin, insoluble in H2O, tightly bound to albumin, not excreted by kindey,
unbound plasma friction (diffuses into tissue, produces toxic injury, ↑ in hemolytic disease of newborn, may lead to neuro damage) causes 4-5: result in increased conjugated bilirubin, soluble in
H2O, weakly bound to albumin, excreted by kidney  dark urine, light/pale stool; can occur dt build up of conjugated or unconjugated bilirubin; if breaking down RBCs too fast, result in build-up of
bilirubin secondary to hemolytic disease CHOLESTASIS unable to move bile, damage to hepatocytes bc buildup in canaliculi bile atresia: bile duct doesn’t form all the way→liver failure in kids
HEPATIC FAILURE sudden & massive hepatic destruction, often end point of progressive liver damage, 80-90% liver function must be lost, life threatening (multi organ failure) special probs: hepatic
encephalopathy & heaptorenal syndrome, can have acute hepatic failure CIRRHOSIS & PORTAL HYPERTENSION lumpy liver due to progressive fibrosis; bp increasing to try to find way out through
rectum, umbilicus, and lower esophagus; cirrhosis impairs blood flow through liver→hepatic portal hypertension→ ascites, portosystemic shunts (esophageal varices, hemorrhoids, caput medusa),
splenomegaly, impaired bf out of liver→ hepatomegaly caput medusa: blue-green lines out of umbilicus, deoxygenated blood mixed w/ bilirubin VIRAL HEPATITS inflammation of liver 2nd to virus; 5
causative agents = hepatitis A-E virus (all different but bind to and infect hepatocytes); permanatent viral infection, asymptomatic; can be acute or chronic HAV & HEV: self-limiting, 2-8 wk
incubation, no carrier state, no chronic hepatitis, no cancer, oral-fecal transmission, not usually in US HAV: common childhood disease in developing counties, adult infection more dangerous,
sporadic infections (oysters), VACCINE HEV: sporadic infection rare, typically endemic & in travelers, ↑mortality rate in pregnant women (20%) HBV, HCV, HDV: carrier state, chronic hepatitis, cause
cancer, parenteral transmission (needles or sex, mother  child in China), present in US; HDV cannot survive w/o HBV HEPATIC STEATOSIS (fatty liver) fat inside hepatocytes, enlarges liver, take up a
lot of alcohol & convert to lipoproteins but cannot clear fast enough to keep up with consumption (reversible), ALT & AST in blood, inflammatory process collagen laid down, if persists →cirrhosis
ALCOHOLIC LIVER DISEASE nodules formed by collagen, acute hepatitis 2nd to excessive alcohol intake, ↑AST & ALT; Hepatic steatosis 90-100%, alcoholic hepatitis (fluid wave, enlarged liver, Mallory
hyaline, portal fibrosis, fatty liver) 10-33%, cirrhosis 8-20% alcoholic cirrhosis: accumulation of collagen, irreversible, nodules of varying sizes are entrapped in blue-staining fibrous tissue, vascular
resistance ↑, bilirubin & bile accumulate in liver  greenish tint HEMOCHROMATOSIS (hereditary iron overload) uncontrolled excess uptake of iron (~1gm/year), limit iron stores by regulating uptake
of iron; male predominance (women get rid of iron through menstruation), most common metabolic genetic disorder- autosomal recessive (0.5%), carriers (10%), carriers predominantly white,
probs 50+ yo; easy to treat: bleed problems: cirrhosis (100%), diabetes 75-80% (iron in pancreas), grey skin pigmentation (75-80%); Bantu siderosis: genetic mutation occurs in Africa, less common,
also recessive Secondary iron overload: transfusions (1 = .25 g), thalassemia- want to give blood bc anemic but give iron overload OBSTRUCTIVE BILIARY TRACT DISEASE secondary biliary cirrhosis:
obstruction of extrahepatic biliary tract, common causes (gallstones, biliary atresia, malignancies of biliary tree or pancreas, strictures from surgery) primary biliary cirrhosis: destruction of
intrahepatic bile ducts dt immune attack, ↑ AP & cholesterol, hyperbilirubinemia late in disease, antimitochondrial antibodies (>90%), often fatal primary CIRCULATORY DISORDERS 4 ways blood can
go wrong way in liver; obstruction w/ outflow: thrombus in vena cava or R heart failure (blood backs up into abdominal cavity  hepatomegaly, splenomegaly, ascites, jaundice) impaired
intrahepatic bf: trouble w/in liver, portal hypertension (splenomegaly, NOT hepatomegaly from cirrhosis) impaired blood flow into liver: liver is fine, portal system can’t drain properly impaired
hepatic artery flow: complication of transplant PRIMARY CARCINOMA OF LIVER uncommon, most liver cancer metastatic; arise from hepatocytes caused by: HBV (earlier you get it, more likely to
get cancer; China has high rate com to US), chronic liver disease (HCV and alcohol), aflatoxin (not common problem), tyrosinemia (rare but 40% HCC), cirrhosis (correlated with hepatocellular
carcinoma but not necessarily a cause); 7 mo survival rate, early HBVgreater HCC rate CHOLELITHIASIS usually asymptomatic until stones move cholesterol stones: fair-forty-female-fertile-fat
pigment stones: made of bilirubin (darker), hemolytic disease↑bilirubingallbladder withdrawing H2Oprecipitation; biliary infection, GI disorders, Asian>Western CHOLEDOCHOLITHIASIS
(gallstones) stones in biliary tree, on the move; if get stuck in one of ducts, it becomes very painful and can prevent bile from exiting liver (bile backs up); lots of pain, can no longer get rid of
bilirubin from liver, so bilirubin levels increase, conjugated bilirubin goes up (… jaundice); probs: ↑AP, abd pain, vomit w/ fatty food, biliary obstruction, jaundice, intracanalicular cholestasis,
swollen liver cells, no necrosis, no fibrosis, pancreatitis (distal blockage of pancreatic enzyme excretion  pancreas autodigests  inflammation), cholangitis (inflammation of gallbladder), hepatic
abscess, chronic liver disease w/ biliary cirrhosis (can’t export anything through bile system, everything backs up and hepatocytes start dying), acute calculous cholecystitis (inflammation) ACUTE
PANCREATITS Pancreas secretes digestive enzymes into duodenum; don’t want pancreatic enzymes to activate in pancreassecreted in inactive form (proenzymes) causes: idiopathic, gallstone
(blockage in ampulla of Vater & can’t secrete pancreatic enzymes), alcohol (will either get cirrhosis or pancreatitis (usually not both)), trauma (accident to pancreas), steroids, mumps & other
viruses, autoimmune, scorpion sting, hypercalcemia, hyperlipidemia, hypothermia, endoscopic retrograde cholangio-pancreatography, drugs MUSCLE FIBERS muscle cell is a muscle fiber, runs
from insertion to exertion, many nuclei (lots of cells came together to form muscle cell), hypertrophy not hyperplasia (↑ # of nuclei) Myofibrils: can run whole length of cell, doesn’t need to;
alternating dark, light bands (sarcomere), dark band-A band w/ M line in middle (A band only myosin, M line where myosin is anchored) light band- I band w/ Z disk in middle (I ban no myosin, Z
disk where actin anchored) Contraction: need Ca & ATP, I band slides over A band w/ Z’s getting closer together (I band gets narrower, A band stays same length); sarco= flesh, myo = muscle
SARCOPLASMIC RETICULUM & T-TUBULE FOR TRIAD SR stores Ca; action potential comes down axon→ depolarization at terminus opens voltage gated Ca channel→ Ca moves into cell→axon
terminus releases neurotransmitter Ach into cleft→binds to Ach gated Na channel on muscle cell→ Na move into muscle cell→cell depolarizes as Na continues to enter→voltage gated Ca
channel opens→ Ca moves into muscle cell from outside via t-tubules→opens Ca-gated Ca channel→Ca comes into cell from SR→contraction MUSCLE CONTRACTION troponin bound to
tropomyosin, 3 parts of troponin (C- where Ca binds, T- bound to tropomyosin, I- ignore), Ca comes in & binds to troponin C→ changes conformation→moves tropomyosin to that actin binding site
is exposed to myosin; myosin releases, repositions, binds & flicks to stop contraction: run out of actin, Ca removed from SR, cell runs out of ATP (ADP used to bind & flick); move 1 actin G per cycle,
10^21 binds & flicks per stride FIBER TYPES slow twitch: Type I (slow oxidative- use O2, not easily fatigues, everyday use) fast twitch: Type IIb (fast glycolytic- infrequently, long breaks between use);
muscles are mosaic of fast & slow, all fibers of same motor unit are same type example: fast twitch dominant- latissimus dorsi, slow twitch dominant- tongue DYSTROPHY pt looks starved, X-linked 
men dystrophin: protein associated with dystrophy; if missing, actin attached to membrane along cell not anchored properly- rips plasma membrane every time person exercises→ inflammation,
sore muscles weaker with every use; expect to find enzymes from muscle inside blood initially but not later when muscle destroyed MYASTHENIA GRAVIS antibodies bind to acetylcholine receptors,
immune system attacks, damages receptor, prevent receptors from working symptoms: weakness or paralysis, droopy eyelids, speech probs, symptoms get worse as day goes on (stored Ach is
used); acetylcholinesterase breaks down Ach- acetylcholinesterase inhibitor diagnostic & treatment MYASTHENIC SYNDROME antibodies against voltage gated Ca channels on nerve
terminals→won’t open→Ca can’t come in & axon terminus can’t dump Ach; acetylcholinesterase inhibitor won’t help; weak in morning and night CURARE from poison dart frogs, works as paralytic,
great neuromuscular block for surgery (must intubate) CLOSTRIDIUM BOTULINUM TOXIN in Botox, Ach vesicles won’t fuse w/ plasma membrane → cant dump neurotransmitters→ no muscle action
 paralysis; long half life CLOSTRIDIUM TETANI TOXIN vesicles keep fusing w/ plasma membrane, muscles won’t relax, causes lock jaw BONE PHYSIOLOGY reabsorbed: bone removed;
hematopoietic stem cells → osteoclasts (fusion of macrophages), undifferentiated mesenchymal cells→other bone cells diaphysis: shaft epiphysis: ends articular cartilage: where bones articulate
at synovial joints, insensitive to pain, regenerates slowly cortical bones: compact, solid, Haversian systems (osteocytes between rings) medullary bone: spongy bone, bone marrow; epiphyseal
(growth) plate: btwn dia- and epiphysis where growth occurs DISORDERS OF SKELETAL SYSTEM arthritis, bursitis, cancer, dislocation, osteomalacia (soft bones), osteomyelitis (inflammation of bone),
osteoporosis, sprain, strain, Tennis elbow kyphosis: curvature of upper back lordosis: curvature in lumbar region scoliosis: s-shaped curve laterally, congenital/developmental OSTEOPOROSIS
compact bones get thinner, trabecular bone gets more spongy & loses strength, loss of bone mineral density, cortical bone continues to get wider; lose 1% of bone material per yr after menopause;
bone turns over every 7 yrs bisphosphates: slow rate of bone breakdown; crush fracture of vertebrae common more common in women: men start out w/ bigger bones, lose bone slower, die
younger PAGET’S DISEASE excess bone turnover, disorganized bone, viral infection/autoimmune?, responds well to biphospate treatment HYPERPARATHYROIDISM too much PTH signals need Ca in
blood→get it from bone→osteoporosis OSTEOMYELITIS wall-off infection w/ bone filled cyst, build new bone (involucrum) around it, do not get bad with proper medical care BONE & JOINT TUMORS
primary is rare (.2% cases .3% deaths), poor survival, usually metastatic, prefer primary; osteosarcoma (cells that make bone), osteoblastoma (early precursor cell), osteoid osteoma (prob not
cancerous), chondroblast (cartilage precursor), chondrosarcoma (cancerous), fibroblast (collagen-producing), reticulum (bone marrow) JOINT DISORDERS noninflammatory joint diseases:
osteoarthritis- dt life-long use (bone on bone rubbing bc cartilage eroded), worsened by: traumatic injury, dislocations, & sprains- destruction of cartilage; glucosamine &chondroitin to prevent, hip
or knee replacements to treat; big joints most affected (hips, knees, back, hands), worse as day goes on, anti-inflammatories, v painful; inflammatory joint disease: rheumatoid arthritisautoimmune attacks joints  destruction, at any age, scaly growth on bone, ulnar deviation, treated w/ immuno-modulators (slows progression, doesn’t cure), subcutaneous nodules around
knuckles; gouty arthritis- diet induced w/ ↑meat (uric acid crystals), big toe 1st, happens suddenly, no broken bone, crystals cause macrophage ruptures, treatment- block production of uric acid;
infectious arthritis (Lyme disease), inflammatory TALIPES EQUINOVARUS common birth defect, needs to be straightened w PT, brace/splint, or surg, caused by lack of space/amniotic fluid in
womb→compression (oligohydramnios) OSTEOGENESIS IMPERFECTA defect in collagen I (deficiency), broken bones, blue eyes- dt collagen defect, treatment: rods to prevent breaks RICKETS Vit D
deficiency, have collagen but not enough Ca++, bone bending, treatment: vit. D SRY sex-determining region of Y chrom, located on short arm outside pseudoautosomal region, converts embryo to
male- wk 9 of gestation ANTI_MULLERIAN HORMONE causes degeneration of female specific structure MALE GENITALS sperm development: spermatogenesis in seminiferous tubules/vesicles of
testes, maturation in epididymis & vas deferens, fully mature by ampulla of vas deferens (storage site); motility via peristalsis; spermatogonia (stem cells)  primary spermatocyte (1 daughter
cell)secondary spermatocytesearly spermatidslate spermatid (1 primary spermatocyte)  4 sperm seminiferous vesicles: filled w/ tubes that make sperm; hold leydig cells, ↑concentration of
testosterone Leydig cells: interstitial cells between tubules, produce testosterone, lipid droplets sertoli cells: growth factors & nutrients for developing sperm, for blood-testes barrier w/ tight junction;
testes = immune privileged area HYPOPHYSEAL CONTROL OF MALE REPRODUCTION LH & FSH are anterior pituitary hormones under gonadotrophin releasing hormone (from hypothalamus) LH:
stimulates Leydig cells to produce testosterone, from ant. pituitary FSH: stimulates Sertoli cells to support sperm production (testosterone helps); exogenous testosterone stimulates – feedback of
hypothalamus ↓FSH & LH (chronic exogenoustesticular atrophy) hCG: human chorionic gonadotrophin stimulates Leydig to produce testosterone similar to LH, can take w/ testosterone to
prevent testicular atrophy, + pregnancy test PROSTATE benign prostatic hyperplasia: prostate grows w/ age, replicate into big nodules starting in central zone, compresses prosthetic urethra early,
digital rectal exam carcinoma of prostate: invades & metastasizes (lung, liver, & bone), ↓mortality rate, arise from peripheral glands, PSA- faulty early detection; US has highest rate STD/STI VIRUSES:
Genital herpes (HSV/HHV): HHV1 = fever sores (trigeminal nucleus); HHV-2 = genital herpes, cannot get rid of it bc infects neurons (dorsal enlargements off sacrum), 90% of adults; HPV: 1/2 = warts
on hands/feet; 6 & 11 = genital warts, not ones that cause cancer; vaccine, burn freeze or acid to remove, smallest/shallowest ulcers; BACTERIA chlamydia (trachomatis): most common STI, 2nd
cause of infertility, 10% women 15-24, chronic inflammation/scarring of fallopian tubes  difficult for eggs to pass through, intracellular, mostly asymptomatic, can lead to PID, treatable difficult to
culture; gonorrhea (Neisseria gonorrhoeae): gram-, pain & burning urination, yellow discharge or asymptomatic, treat w/ antibiotics (penicillin); syphilis (Treponema pallidum): rel uncommon,
spirochetes, small painful ulcerations, fairly easy to treat; chancroid (Haemophilus ducreyi): large, deeper ulcerations than herpes/syphilis; protozoa: Trichomonas vaginalis: asymptomatic in men
(clears ~2 weeks), ↑vagina pH infections in women (E.coli, candida); Ectoparasites: Scabies: warm damp areas, skin lesions  itching; Pubic lice: different from head lice, itching OVARIES/EGGS
eggs in ovarian cortex follicles: primordial follicle (surrounded by 1 layer of squamous epithelial)primary follicle (cuboidal/columnar cells around egg) secondary follicle (secretes factors that
suppress others)graffian follicle (fluid-filled antrum); born w/ 2 mill eggs layers of Graafian follicle: innermost- granulosa (converts androgens to estrogen, spike at mid-cycle  follicle rupture
basement memtheca intern (produces androgens)theca extern; cumulus oophorus-cells that surround egg even after release corpus luteum: follicle of month, produces primarily progesterone
after ovulation zona pellucida: shell of egg that sperm digests chorion: fetal contribution to placenta, produces hCG  stimulates corpus luteum to produce progesterone if fertilization occurs
MENSTRUAL CYCLE follicular phase: proliferative phase before ovulation, follicle develops in ovary & endometrium proliferates luteal phase: secretory phase after ovulation, follicle becomes corpus
luteum & endometrium awaits implantation; big spike in LH & FSH ↑estrogen in follicle (+ feedback of estrogen to hypothalamus)rupture/release of egg; corpus luteum corpus albicans if no
fertilization FEMALE HORMONES LH: stimulates theca cell to produce androgens, causes follicle to turn into corpus luteum FSH: stimulates granulosa cells to convert androgens to estrogen & support
egg development; - feedback for FSH & LH to hypothalamus during follicular growth exogenous estrogen: inhibits FSH↓estrogen (mechanism of birth control- progesterone allows endometrium to
grow & placebo allows shedding of endometrium) progesterone: supports endometrium, ↓during period hCG: produced by placenta if implantation, maintains/stimulates corpus luteum to produce
progesterone (looks like LH & binds to LH receptors), ↑ during pregnancy, binds to TSH and takes over work, ↓ during pregnancy GONADOTROPES In utero & after birth: ↑LH & FSH (sexual
differentiation) childhood: ↓LH & FSH after puberty: cyclical pattern, ↑w/ each cycle as menopause approaches post menopause: ↑FSH & LH, ↓estrogen & progesterone CERVIX columnar cells in
uterus, stratified squamous in vaginasquamouscolumnar cells in cervix CERVICAL CANCER HPV: 16 & 18 ↑ risk of mutations and developing cancer cells, blocks retinoblastoma/P53 proteins,
usually no effect but sometimes infect cells; occurs where columnar epithelium of cervix meets squamous epithelim of the vagina; also cancer in anus, vagina, penis, mouth, throat; vaccine
prevents viral infection; 100% cervical cancers assoc. with HPV; treat with surgery pap smear: necessary bc 30% HPV not covered by vaccine ENDOMETRIOSIS endometrial cells in pelvis grown &
slough off each month, spreads via retrograde fallopian tubes, blood/lymph; v painful treatment: put on birth control w/o placebo pills (no period) TUMORS Leiomyomas: benign tumor of uterine
smooth muscle, common, bleed, ↑w/ age, severe versions not viable with pregnancy leiomyosarcomas: malignant version, much less common; endometrial cancer: cancer of epithelial layer
(usual uterine cancer), most common of reproductive tract, ↓ mortality, bleeding in post-menopausal women, easy to diagnose; PROLAPSE Uterine: muscle & ligament suspension weakens, uterus
starts to descend into vagina, painful; cystocele (bladder), rectocele (rectum) SALPINGITIS salpinx= fallopian tubes, open at both ends; inflammation dt infection; can lead to ectopic pregnancy dt
damage and scarring, usually part of PID: inflammation of fallopian tubes or ovary caused by endometriosis, chlamydia, gonorrhea, TB; POLYCYSTIC OVARIAN SYNDROME etiology: ↑ LH & ↓FSH 
androstenedione into circulation  converted to estrone (in peripheral fat)  - feedback to hypothalamus ↓FSH; lead mature follicle never ruptures, become cysts; common in obese women w ↑
insulin, metabolic syndrome, diabetes symptoms: irregular or no menstruation, excess androgen, enlarged ovaries w/ cysts, ↑hair growth, infertility treatments: birth control to regulate LH & FSH, 50%
chance of pregnancy after several months OVARIAN TUMORS happens @ any age, ↑w/ age, ↑ mortality dt late detection, if producing hormones  earlier detection, ↑w/ BRCA 1; TERATOMA germ
cell tumor, partially differentiates (can grow hair and teeth); can occur in men/women @ any age, typically in ppl born w them; don’t become cancerous @ high rate, ECTOPIC PREGNACY outside
body of uterus, unable to support placenta dt insufficient blood supply, destroys tissue it resides in, can cause lower abd pain, exsanguination (pain & bleeding to death) HYDATIDIFORM MOLE
complete mole: no maternal DNA & 2 sperm  diploid maternal DNA, lots of hCG, no fetus, must remove partial mole: norm egg w/ 2 sperm (triploid), not viable PRE-ECLAMPSIA 5-10% of
pregnancies, chorionic villi didn’t penetrate far enough into endometrium↓nutrients to fetus triad: htn, proteinuria, edema; inadequate blood flow to fetusinadequate development of placental
spiral arteries, 3rd trimester; can become eclampsia: involves seizures, can be fatal, seldom occurs, premature delivery @ 35 weeks AMENORRHEA ↑prolactin: nursing child or look at sella turcica for
pituitary tumor; 10% body fat: need fat for baby ↑TSH: prob hypothyroidism, give progesterone for wk then withdraw ↑FSH & LH: prob w/ ovary or Turner’s ↓FSH & LH: prob w/ anterior pituitary, look at
sella turcica BREAST CANCER 1/2 in upper outer quad (tail of spence), most = ductal carcinoma, BRCA1 85% risk; if gets to avillary lymph nodes  remove  lymphedema; invasive ductal
carcinoma, get fat necrosis that attracts Ca  benign calcifications, detectable CASE STUDIES: Iron Deficiency Anemia: HEU,17F fatigue, weakness, SOB, headache. RBC 4.8. microcytic,
hypochromic RBCs Sickle Cell Anemia:SK,48F,black, pain despite oxycodone use, sharp:elbow,knee,abdm, fever, blood exchange transfusion, hgb8.2, hct23.5%, retic12.4%,WBC11.4 [2]: DC, 5M,
black, chest pain, tachycardia/tachypnea, SOB, T100.3, acute chest syndrome, hgb8, hct28%, anemia, splenectomy Sickle cell crisis: KS, 3F, acute onset chest pain, dyspnea, fever, flu symtpoms,
multiple hospitalizations r/t anemia RR42, BP92/52 Acute Idiopathic Thrombocytopenic Purpura: MM, 6F. fever & vomiting. easy bruising & heavy bleeding. scattered petechiae over body.
extremely low platelet count Coumadin overuse: DA, 61M. changed mental status. acute right subdural hemorrhage w/ chronic head hemorrhage. INR 9.0. pmh: obesity, COPD, HTN, CVA, PVD, MI,
A-fib (Coumadin), Gout, DVT, & left BKA. melena stool. PT: 26.8 sec. Glucose: 147. BUN: 94, Creatinine: 8.92, Platelet: 139, RBC: 2.50, Hgb/Hct: 6.6/ 22.9%,+ Fecal Occult Blood Test. enlarged heart. b/l
atelectasis. pleural fluid. worsening Lvent function. EF <15%. pulmonary htn Severe Anemia (post liver transplant): JB, 17M, Hct/Hgb of 18.9&6.8. left flank pain. multiple signs of bruising. pmh: liver
transplant, distal splenorenal shunt 2nd to portal hypertension. BP:100/56. Ultrasound of left flank: iliopsoas hematoma. WBC 1.8, RBC 2.06, Hgb 6.8, Hct 19.1, MCV 92.7, MCHC 33.1, RDW 35.7, Plt 40,
PT: 17.4, INR: 1.5, PTT: 39.2. AST 63, ALT 94, Alk Phos 243, GGT 40, direct bilirubin 0.2, total bilirubin 2.3 ALL: CH 25F fatigue & body pain, stress. petechiae entire body. large bruises, bleeding from nose
&gums. hemoptysis. ↑WBC. ↓platelet. Philadelphia chromosome AML: KG 31M flu-like sxs. fatigue, tooth pain, wt loss. N/V, blood in vomit & diarrhea. WBC=127,000 Hgb 6.6, Hct 19.7, Plts 47, Albumin
2.5, LDH 729. Uric Acid 7.4. DLBCL: KG 42F. flu-like sxs. swollen, non-painful LNs in neck, armpits, groin. nagging cough. Back/ab pain. diarrhea. night sweats, fevers & wt loss. hx colorectal can cer,
dm, alcohol/drug use. [2] 28M. ab pain. hx: HIV, hep B. CT scan: soft tissue masses&lymphadenopathy. creatinine 1.7. partial obstr of R ureter. Hodgkin’s wt loss. chest tightness. night sweats, fatigue.
non-productive cough, fever, ↑WBC, (esp lymphocytes), ↑ESR. chest x-ray: 12cm mediastinal mass. Reed-Sternberg cells. [2]EK 21F. enlarged cervical LN. MRI: suggests lymphoma. biopsy: ReedSternberg cells Epstein-Barr virus. [3] RJP 50M cough, weakness, nausea. hx: ulcerative colitis post ileostomy & anal sq cell carcinoma status post radiation. HR 114, BP 110/70. H/H 10.8/35.3, WBC
15.9, Bicarb 16 BUN 33, creatinine 1.Multiple Myeloma: SK 30F back & L side rib pain. tender to palpation in L U chest, tenderness on the L scapula. fever, HTN. Anemia- Hgb 8.3 & Hct 24.3. Bone
scan: plasmocytoma CT scan: body lesions. free Kappa Light chain urine ↑protein. ↑IgG. ↑gamma globulin. 20% atypical plasma cells. plasma cell neoplasms Non-Hodgkin’s lymphoma: JM 57M hx
myasthenia gravis. fatigue, weakness. ↓BP. retroperitoneal & inguinal lymphadenopathy Post Transplant Lymphoproliferative Disorder-E.R., 2 F, fever over past 2 wks, lymphadenopathy PMH-biliary
atresia, Kasai procedure, acute rejection post transplant-had high Epstein-Barr-virus level Embolic CVA: (ischemic stroke)C.O., 81 F, cooking, slurred speech, L side weakness, A&Ox2, past cardia
stents Subarachnoid Hemorrhage: C.M., 66 F, “worst headache of her life”, nausea, ^BP, not taking antiHPT meds [2] K.M., 52 F, sudden headache, nausea, febrile, photosensitivity [3] C.D., 41 F,
frontal headache, vomitus, grand mal seizure Subdural Hematoma:unresponsive infant-8 m.o., irreg, shallow breaths, posturing, pupils sluggish, ant fontanel tense, generalized seizure, PMH
occipital skull fracture [2] K.W., 83 F, confusion, slurred speech, 3/5 strength-RLE/RUE, worse since fall 3 wks prior Transient Ischemic Attack (TIA): 73yrs. slurred speech, L facial droop. hx: DM, HTN,
pontine infarct, TIA, & aortic stenosis. BP 233/110. HR 55 Meningitis 4wks. potential seizure. tachpnea, expiratory grunting. slow cap refill. exaggerated startled reflex. bulging anterior fontanel. fever.
lumbar puncture: CSF purulent, yellow in color, & cloudy, growth of Streptococcus beta-hemolytic, group B. glucose: 0 mg/dL, protein: 338 mg/dL, appear. cloudy AB, CSF RBC 3 /mm3, CSF WBC
77/mm3, polys 53 %, lymph 26%. Gram+ cocci chains. [2] 34yrs. fever, headache, stiff neck, photosensitivity. Multiple Sclerosis: 25yrs. pain behind eyes. weakness &pain in L upper & lower
extremities. hx: fibromyalgia, multiple sclerosis w/ episodes of optic neuritis. drift in left upper extremity. ↓ sensation to touch & pinprick below ankle on LLE. Positive paresthesias to touch on LUE&LLE
[2]: RJP, 26F, Came to ER w/ numbness from hips down, difficulty walking, feet have been numb for a few weeks. Abnormal lab: WBC-15. MRI of brain showed plaques&scaring Amyotrophic Lateral
Sclerosis 54yrs. slurred speech & dyspnea. consisted muscle weakness & unsteady gait. acute resp. acidosis. + babinski sign. hx: HTN. p H 7.28, PaCO2 55, HCO3 27. Negative MRI, CT, lumbar
puncture. [2] 67yrs. hx: HTN, arthritis, heartburn. wasting of hand muscles, muscle twitching, wt loss. ↑progressive weakness, SOB, loss of appetite. lethargic. BP 170/85. pH 7.115, PaCO2 167.5, PaO2
115, HCO3 52.6, B/E 14. EMG confirmed ALS. Creutzfeldt-Jakob Disease 49yrs. ↓ mental status & ↑seizure activity. Dementia 82yrs. hx: DM2, HTN,&hyperlipidemia. nursing home. progressive
dementia. difficulty w/ short term memory. more accident prone. disoriented. can’t open eyes/follow commands. slow neuromuscular reflex. progressive demensia. WBC 20. CT: holes in brain
tissue. CSF: +14-3-3 protein. MRI: holes in brain. EEG: triphasic waves w/ ↓ neuronal activity. Diabetes insipidus: 33yrs. headaches. pituitary tumor removal. increase urine output. severe thirst.
Glioblastoma: 56yrs. tonic-clonic seizure. obese w/ hx: HTN, hyperlipidemia, hypogondaism, obstructive sleep apnea &DM. altered consciousness. not responsive to painful stimuli. CT: frontal
hypodensity w/ mass effect & shift. mass reached across multiple hemispheres. Lumbar Stenosis 72yrs. difficulty walking r/t weakness& parathesis in legs. low back pain. bowel incontinence. hx:
DM, HTN, overweight, cervical laminectomy w/fusion, ulnar nerve entrapment release surgery, hysterectomy, & 2 ectopic pregnancies. MRI: multilevel degenerative disk disease & stenosis from L2
to L4-5 junction. MVC w/TBI 19yrs. motor vehical collision. b/l nonreactive pupils. pH 7.3, PaO2 150, PaCO2 45. CT: cerebral edema, possible diffuse axonal injury. Neuroblastoma: 12mos. no wt gain.
ht velocity ↓. intermittent liquid stool w/ hard inbetween. fever. thin arms/legs, distended belly. light palpation of ab gives crackle sensation, deep&superficial masses. Hgb 9.2g/dL, Hct 31%, LDH
197units/L, Ferritin: 243ng/ml, VMA 72 μg/mg creatinine, HVA 99 μg/mg creatinine. most common tumor in infants. Appendicitis in Pregnancy: 22yrs. RLQ pain. 26wks pregnant. tender ab to
palpation all over. ↑pain on L sided palpation. ↑ WBC 24,000 w/ ↑ segs. fever. mild dehydration. ultrasound: inflamed appendix. Appendicitis 10yrs. HR 124, BP 92/64, ab pain in RLQ. nausea. ↑ WBC.
rebound tenderness in RLQ. Colorectal Cancer: 54yrs. ab pain, ↓ appetite, wt loss. changes in bowel patters, frequent blood in stool. hbg&ht low. hx: HTN, DM2. colonoscopy revealed polyps. bx
confirmed adenocarcinoma of descending colon. Crohn’s Disease: 39yrs. ↑ab pain. anorexia, N/V, diarrhea, constipation. BP 110/70. WBC&platelets ↑. ↑ ESR/sed. rate. [2] 49yrs. diarrhea. ab
pain/cramping. fever. hx. crohn’s. CT: ↑inflammation. Esophageal Varices & Blakemore Tube: 54yrs. hx: alcoholism, Hep C, Cirrohsis, upper GIB, varices s/p failed TIPS procedure. altered mental
status. hepatic encephalopathy w/ Ammonia 60. N/V, blood. pale, jaundiced. BP 60/30, HR 124. Na: 133, K: 3.5, BUN:19, Creatinine: 0.8. WBC: 7.2, Hbg: 4, Hct: 10, Plts: 20, INR: 3.4. Albumin: 2.0,
Alkphos: 300, AST: 230, ALT: 120, TBili: 4.5 Esophageal Varices in Pregnancy 35yrs. 39wk pregnancy,. contractions, vomiting. Hx: hep c, alcoholism, IV drug use, preganancy induced HTN. BP 90/50.
vomiting blood. emoglobin: 6, Hematocrit: 16, Platelets: 50, PT: 20 PTT: 40. Albumin: 4 AST: 23 ALT: 56 GVHD 26yrs. dx w/ Acute Myelogenous Leukemia. diarrhea, vomiting, ab pain. 22days past
allogenic bone marrow transplant. WBC 1.0, ANC 0.4, Hgb 6.8, Hct 22%, Plt 12,&positive fecal occult blood test. post endoscopy: mucosal edema & diffuse bleeding throughout entire GI . Crypt cell
necrosis. Postop Ileus: 14yrs. 4 days past Posterior Spinal Fusion. hx: Adolescent Idiopathic Scoliosis. hypoactive bowel. N/V. Na=129, K=3.6, Hgb= 8.3. xray: ↑ diaphragm & small intestine dilatation.
Small Bowel Obstruction adhesions: 42yrs. ab cramping, N/V, constipation. xray & CT scan: small bowel obstruction due to mechanical obstruction from fibrous tissue. Small Bowel Obstruction:
71yrs. ab pain&distention, vomiting, constipation. hx: HTN, CHF, CAD, coronary artery bypass graft. dehydrated, hypokalemic, & hypochloremic metabolic alkalosis. xray: air/fluid levels. Ulcerative
Colitis 21yrs. frequent diarrhea&cramping w/ small amounts of blood. BP 105/70. WBC in stool. colonoscopy: inflammation &reddened mucosa of rectosigmoid colon. Bx: inflammation of
crypts.Acute Cholecystitis: 58yrs. hx: HTN, DM2, & obesity. nausea & abd pain to RUQ. ab soft, tender, mild distention. WBC 18. ultrasound: inflamed gallbladder wall & stones. Acute Necrotizing
Pancreatitis 24yrs. ab pain radiating to back. N/V. alcoholic. ab distended &firm. HR120, BP 90/56, RR29, fever. Amylase-625 U/L, Lipase-1295. leukocytosis, hyperglycemia, ↑ alkaline phosphatases,
conjugated bilirubin,&gamma-GT. CT: pancreatic fluid collection, pancreatic necrosis. Biliary Atresia: newborn baby. jaundiced. darker urine & acholic stools. total bilirubin was ↑&direct bili ↑. GGT
also ↑. HIDA scan: complete obstruction of bile flow in common duct. Biliary Obstruction (cholesterol stones) 2yrs. jaundice, itching, acholic stool. ALT- 53, AST- 38, Alk Phos- 393, Total bili- 7.4, Direct
bili- 6.8, GGT- 998. total cholesterol 518. ERCP: removed gallstone composed of cholesterol. caused obstruction in bile flow. Biliary Obstruction (post transplant): 1yr. inpatient transplant unit w/ fever,
mild jaundice, pruritus, & pale stools. ALT: 198, AST: 293, ALK Phos: 780. GGT1864, T. Bili 6.9, D. Bili: 5.8, Albumin: 3.6. PTC: dilated & blocked bile duct. Chronic Hepatitis C: 35yrs. drunk, R ab pain,
N/V, fatigue, itching. hx: chronic alcohol abuse, former drug use, hepatitis C, & HIV. fever, jaundice, ascites. + Hep C antibodies. AST/ALT ↑. prothrombin time was prolonged;
hyperbilirubinemia,&hypoalbuminemia,&↑ ammonia levels. Cirrhosis of Liver: 57yrs. ab pain, fatigue, nausea. jaundice, ascites, gynecomastia. anorexic. hx: ETOH abuse & HTN. enlarged
liver&spleen, multiple nodules on liver. Fulminant Liver Failure (Tylenol OD) 16yrs. confused, combative. battled depression. actively vomiting, jaundiced, altered consciousness. CT: cerebral
edema. Creatinine: 1.13, BUN: 20, D. Bili: 4.4, T. Bili: 7.8, Alk Phos: 158, Albumin: 2.7, T. Protein: 4.9, AST: 635, ALT: 2,516, Phos: 1.8, Ammonia: 112, Amylase: 49, Lipase: 587. GSW to abdomen: 16yrs.
multiple gunshot wounds to the head. HR 120. BP 80/50. RR 30. RUQ wounds, minimal bleeding. response ↓. H&H 5/16, coags ↑. Hyperbilirubinemia in Newborn preterm baby. Rh sensitivity. on
ultrasound had fetal hydrops. O2 sat 60%. jaundice. X2 total billirubin. extra-uterine exchange transfusion Liver transplant full-term infant. seizures, hypoglycemia, lethargy, poor PO feeding &
vomiting, fever& respiratory instability genetic defect causing urea cycle disorder. rise in nitrogen → ammonia in blood/brain. Pancreatic Adenocarcinoma: 59yrs. 2 polyps & mass in ascending
colon. benign. severe ab pain. MRI: mass. jaundiced. CT: mass involving pancreas. constipation. Pancreatitis: 26yrs. ab pain, N/V, dark urine. UA + blood. CT: edema around pancreas. Lipase:
15000. Primary Sclerosing Cholangitis: 15yrs. jaundic. Alk Phos- 497 unit/L, AST- 88 unit/L, ALT- 62 unit/L, Total bilirubin- 4.6 m/dL, Direct bilirubin- 3.4 mg/dL, GGT- 163 unit/L, WBC- 16 k/uL. slowly
increasing liver function tests. fevers. itchy. MRCP: narrowing of small branches of bile duct. Bacterial Vaginosis 21yrs. 36wks pregnant.↑vaginal discharge, vaginal itching & odor. + whiff test & clue
cells. pH = 5 [2] 18yrs. preterm contractions. hx: genital herpes, asthma. resident notices fishy smell & discharge. clue cells&+ whiff test. Breast Cancer 44yrs. non-tender nodule on Rbreast. family hx:
breast ca. firm, mobile. mammogram: dense breast tissue w/ possible architectural distortion, no malignant calcification. ultrasound: irregular lump. guided needle bx: infiltrating ductal carcinoma
with a small area of ductal carcinoma. Breast Mastitis: 28yrs. throbbing breast pain, breast swelling,&redness on Lbreast. fever, fatigue, chills. hx: spontaneous vaginal delivery. more pain w/
breastfeeding. cracks on nipples. hot, painful erythematous lobule L outer quadrant of Lbreast. discharge. subscapular& brachial LN inflamed& palpable, mobile, non-tender. discharge revealed
Staphylococcus aureus. Chlamydia: 18yrs. 2 sex partners, unprotected. reg periods w/ spotting in between. genital exam: inflamed cervix, bleeds easily w/ discharge. + NAAT test for Chlamydia.
pH 4.2. Endometriosis: 17yrs. severe menstrual cramps. painful 1 st period. occasional pain w/ sex. CBC mild anemia. ultrasound: physiologic free fluid in the cul-de-sac, uterus heterogeneous
myometrium may indicate adenomyosis. laparoscopic procedure: reddened “spots” of endometrium on uterus, fallopian tubes, & ovaries. Gestational Diabetes: 32yrs. 2nd baby. ↑hunger & craving
of sugar after eating. lethargy/fatigue. glucose tolerance test: 182mg/dL at 1-hour, 158mg/dL at 2-hour,&143mg/dL after 3-hours. [2] 30yrs. ↑ blood glucose, glycosuria. pregnant, 24wks. occasional
nausea, ↑ fatigue. glucose: 350 HELLP Syndrome: (hemolysis, ↑ liver enzymes, ↓ platelets). 42yrs. pregnant, 25wks. headache. blurry vision, edema in face/hands. hx: HTN, DM, obesity. ↑ BP. AST
225, ALT 375, platelets 75, LDH 610, proteinurea (6388mg). [2] 27yrs. pregnant. gave birth. H&H 9/36%; Platelets 100, ALT 150, AST 200, uric acid 7.2. Hyperemesis Gravidarum: 38yrs. pregnant. N/V, wt
loss. Itching red rash on hands, feet, torso. poor skin turgor, dry lips, puffy eyes. Hgb 9.4mg/dL, Hct 28.2, MCV 80.3FL, MCH 26.7pg. Lactic Acid, Blood – 0.6mmol/L. Sodium- 136mmol/L , Potassium 3.5mmol/L, Chloride- 96mmol/L. Alkaline Phosphatase-149, total protein-6.2, albumin-2.6. UA Specific Gravity 1.035. UA WBC 16. UA Leukocyte Esterase–large. UA protein-100. UA Ketones-10. Bile
Acids-12 Intrahepatic Cholestasis in Pregnancy: 32yrs. preg. itching. dark urine. Hct –33%, Platelets117, Bile Acids ↑. ↓ BP. dx w/ cholestasis b/c ↑ enzymes& bile acids, & itching.Mittelschmerz: 24yrs.
pain in lower R ab. vomiting. pain also occurred on L side. mild vag bleeding&discharge. pain associated w/ ovulation. Polycystic Ovary Syndrome 17yrs. irregular menses, heavy bleeding. acne.
xs hair on face. fasting blood sugar: 129. total cholestero: 205. H&H 12/38. family hx: PCOS. blood tests: testosterone, FSH,&LH levels. ultrasound: cysts on ovaries. Pregnancy Induced HTN (PIH) 31yrs.
pregnant. BP of 130/90, proteinuria. headaches, blurry vision, upper ab pain. Preterm Labor 27yrs. pregnant. hx preterm labor. contractions 5-10 mins, ab/back pain. contractions increasing. Uterine
Fibroid Affecting Pregnancy: 34yrs. pregnant. c/o pelvic pain. ultrasound: intramural fibroid/leiomyoma. Irregular contour of uterus. closed cervix. Uterine Fibroids: 46yrs. menorrhagia &
dysmenorrhea. anemic w/ H&H of 10.0 g/dL & 30.5%. enlarged uterus. ultrasound: fibroid tumor. opts for total historectomy . [2] 44yrs. menorrhagia. lower ab discomfort. given iron IV. hx: chronic
anemia, menorrhagia, & myomectomy 11yrs ago. palpable uterine fibroids. hbg 7, hct 21. Uterine Rupture: 32yrs. preg. contractions q 2-3 w/ pain. blood in catheter. ↓fetal HR]
INSULIN strong growth factor (muscles); brings glucose into cell (fat & muscle cells); use glucose to make ATP or store as glycogen or fat for later; ↑ protein synthesis to make muscle; ↑fat synthesis
to store excess energy; suppress glycogenolysis & lipolysis;↑ sodium ATPase pump (if ↑ serum potassium: give insulin to turn on the pump, follow w/ glucose to prevent hypoglycemia); ↓appetite, ↓
glucagon; ↑glucose uptake by muscle, fat,↑ glycolysis, triglyceride synthesis, amino acid uptake, protein synthesis GLUCAGON hormone of starvation, promotes mobilization of stored energy to
maintain blood glucose, stimulate glycogenolysis GETTING DIABETES type 1: environmental trigger→ anti-islet cell antibodies attack beta cells of pancreas (where insulin is made) → progressive ↓
of insulin release → ↑glucose, ↑ glucagon � ketoacidosis common (leads to fruity breath); type IV hypersensitivity; over time have loss of normal glucose tolerance with loss of beta cells (cannot
produce enough insulin to keep up with body’s demand for insulin); occurs during times of hormonal flux type 2: muscle & fat less responsive to insulin � pancreas produces ↑ insulin, maintains
blood glucose, causes hyperinsulinemia � insulin sensitivity ↓ progressively, hyperglycemia results � Beta cell destruction & loss of insulin production; there is a resistance to insulin by insulinsensitive tissues; insulin intolerance = not taking more glucose from insulin because already have a lot of it, should either use it (aerobic exercise) or take in less glucose Treatment for Diabetes:
Anti-hypertensive drugs (ACE inhibitors, angiotensin receptor Blockers (ARB) HYPERGLYCEMIA type 1: no insulin release/creation, ketoacidosis bc of ↓ insulin & ↓ glucagon; type 2: tissue resistant to
insulin, cells aren’t taking it up TYPE II ↑ glucose ↑insulin ↓ glucagon, 90% of diabetic cases, fasting blood glucose: Over 100 mg/dl = pre-diabetes, over 126 mg/dl = diabetes GESTATIONAL
previously undiagnosed diabetes during pregnancy, ↑ risk of future gestational diabetes & type II, caused by chorionic somatomammotropin & predisposition ORAL GLU TEST normal result ↓ in blood
glucose over time, diabetic response= blood glucose remains ↑, plasma glucose > 200mg/dL after 2 hrs = excess HbA1c- GLYCOSYLATED HEMOGLOBIN glucose sticks to proteins � glycosylation;
measures avg blood glucose over time (2-3 months), shows how well diabetes is being controlled; glucose stuck to hemoglobin HbA1c; 4-5% = normal, <7% = good for diabetic; over time can
cause inflammatory damage due to number of macrophages breaking down Advanced Glycosylation End Products ACUTE COMPLICATIONS hypoglycemia- type 1 ONLY too much insulin taken,
resolves with sugar intake diabetic ketoacidosis- type 1 not using insulin & glucagon ↑, run out of glucose and use free fatty acids for fuel � urinalysis positive for ketones, leukocyte esterase,
nitrites, & WBC plasma glucose: 455 mg/dL. Anion gap: 18, fruity breath HyperosmoticHyperglycemic NonKetotic Syndrome/HHNKS- blood glucose so high that ↑ blood osmolarity, cells shrink (type
2) CHRONIC COMPLICATIONS nonenzymatic glycosylation – happens w/ ↑ blood glucose: microvascular- diabetic retinopathy (arterioles leak into retina causing blindness), nephropathy
(glomeruli leak causing kidney fail), cardiomyopathy; macrovascular disease – hardening of large blood vessels (CAD, MI, stroke, peripheral artery disease) � arteries are clogged � less blood �
heart and brain starved ; ↑ sorbitol – acts as osmotic agent& attacks nerve cells & lens proteins – causes numbness, pain, & cataracts; other- glaucoma & infection, peripheral artery disease,
coronary artery disease, kidney failure; infections due to poor circulation: gangrene, amputated feet; neuropathy: schwann cells get more glucose, swell up, impinge/impede function
LINICAL C ASES:
Diabetes: JA 27F, weight loss, drinks 1L water/day, frequent urination every 2-3 hrs, ↑glucose; Diabetic Ketoacidosis (DKA): LW 14F, fatigue, thirst, frequent urination, change in breath
odor, nausea, vomiting, disorientation, ↑glucose; [2]: MB 28F, weakness, vomiting, PMH (IDDM), ROS + polyuria, polydipsia (thirst); dysuria, ↑blood glucose, high anion gap; [3]: EC 15F, vomiting,
headache, ab pain, trouble catching breath, kussmaul breathing (hyperventilating), fruity breath odor, HR 115, BP 90/50, RR 3 4, O2 sat 94%, ↑glucose, large ketones in pee, pH 7.3, ↓bicarb/Na;
Gestational Diabetes: CG 32F 2nd baby ↑hunger sugar craving after eating. lethargy/fatigue. glucose tolerance test: 182mg/dL at one-hour, 158mg/dL at two-hour, and 143mg/dL after three-hours.
[2] KW 30F ↑blood glucose, glycosuria. 24wks pregnant, occasional nausea, fatigue. glucose: 350. Hyperosmolar Hyperglycemic Nonketonic Syndrome (HHNKS): NF 72M, found unresponsive, GCS
of 3, ↑glucose, PMH of HTN, Diabetes II, alcoholism, ↓Na, ↑BUN/ creatinine/osmolarity. Uncontrolled Diabetes Mellitus type 2: CC 46F, homeless, pain in left/foot, chills, obtunded, ↑RR, ↓BP, edema,
ulcerations, dark blue/black skin, wounds had foul brown-red/puss discharge, crepitus on foot& ankle, ↑BUN, ↑↑creatinine, ↑glucose, ↑WBCs, ↑K+Atrial Septal Defect: DC 2, tachycardia, tachypnea,
pallor, ↓ Hbg, Hct, murmur Tetralogy of Fallot: AB 23; retrosternal chest pain (sharp, non-radiating, ↑ by strenuous activity) 19 mo duration; dyspnea; occas palpitations assoc w/ dizziness & syncopal
attacks; cyanosis, stage 4 clubbing; systolic thrills, pansystolic murmur over parasternal, ej systolic murmur over pulm area; enlarged shaped <3 w/ pulm oligemia; R ventricular hypertrophy,
inverted T-waves, non-restrictive ventricular septal defect Patent Ductus Art: JR 2 mo F; poor feeding; ↓weight, tired; NAD; ↑RR, crackles in lungs, HR 140 w/ cont. murmur Acute MI: C.L. 65 male;
chest pain “radiating into left arm & jaw;” like chest being stepped on; dyspnea Cardiogenic Shock:TG 65F Rapid Response; overweight; diaphoretic, jaw pain, need O2, tachycardic, Code Blue;
vent fib; patient immed shocked; 90% occlusion to the proximal LAD MI+Cardiogenic Shock: KM 73M; chest pain, complete heart block w/ permanent pacemaker; diaphoretic, SST segment
elevation; ↑cardiac enzymes; given cardiac catheterization; EF: 25-30% STEMI: ZP 58M; chest pain moving to L arm & neck “elephant sitting on chest”, nausea, vomiting, dizziness, HR: 60, RR: 24;
history of MI w/ 2 stents placed; pale skin, diaphoretic, evidence of jugular vein distension when inhales deeply Silent MI: EO 78F; gen surgery floor; controlled A-fib; 4 beat run of vent tachycardia,
ST ↑, ↑troponin MI: IP 64F; new chest pain (substernal, radiating to shoulders/ back), diaphoretic, hx of CAD, pulse 88, RR, 22; ST seg ↑ CHF: LY 27F 8 days post c-section, productive cough w/ pinktinged sputum for 1 wk, labored breathing, diminished breath sounds bilat in base lungs, BP 138/90,RR 28,Temp 98.4 Lab Values- D-Dimer 2.85 ProBNP 750, enlarged <3, bilat pulm edema, L vent
hypertrophy CHF-2: TA 70F palpitations, crackles over bilat lung bases, non-productive cough, ankle edema & anxiety; PMH of diabetes, obesity, HTN, MI, & smoking HR 111 BP 140/80 RR30 O288%.
EKG - sinus tachycardia, enlarged cardiac silhouette / bilat pleural congestion. BNP 900 CHF-3: LW 66F fatigue, 20lb wt gain over 6 wks. S1, S2, S3 sounds, crackles bilat in base of lungs, 3+ pitting
edema to bilat upper / lower extremities. PMH- HTN, hyperlipidemia, hysterectomy BP165/78 HR 118 RR 26, cardiomegaly, fluid in lungs, vent hypertrophy w/ ej fr= 35%. Labs: NA 130 BNP 750 CHF
exacerbation: RE 67F, bilat lower edema, 5 lb wt gain in 1 wk, 3 pillow orthopnea, bilat crackles, 3+ bilat lower edema. PMH-type 2 diabetes, HTN,BP 152/84 RR 26 SpO2 84 %. enlarged heart w/ fluid
in lungs. BNP=1400 Troponin-0.2 Ej fr 30% LVAD: NJ 43M, R h&ed; hx of non-ischemia cardiomyopathy, HTN, hyperlipidemia, C/O 1 mo worsening SOB, orothopnea, lower extremity swelling, fatigue;
neck supple, L jugular vein distension; distant <3 sounds, s3 gallop, LE edema BP: 101/82, HR 90, RR 20 CABG: 65F L h&ed, sudden severe chest pain 10/10 radiating to L jaw, not relieved by rest,
diaphoresis BP 157/81 HR 55 Temp 35.9 C SpO2 100% on oxygen. PMH-HTN, L renal malignant mass post L laparoscopic nephrectomy, hypothyroidism. EKG- L ventricular hypertrophy w/ wide QRS &
repolarization abnormality. Lab values: BUN 22, creatine 1.5, Cl- 109 Hct 33% RBC 3.27 Hgb 10.6 WBC 5.5 troponin .424, cholesterol 225. CAD, ejection fraction 30% Aortic Valve Disease: KS 64M
tightening of chest, lightheadedness, “almost passed out”, grade V murmur @ 2nd ICS w/ thrill radiating to L sterna border , diaphoretic, biphasic pulse in carotids & faint upper /lower extrem pulses,
S4 heard L ventricular heave, crackles bilat. BP-140/110; narrowed PP, L vent hypertrophy, aortic valve calcification, aortic stenosis Aortic Valve Replacement: 93M R h&ed, fatigue, orthopnea,
paroxysmal nocturnal dyspnea, bilateral crackles, systolic ejection murmur. BP 145/86 HR 96 C SpO2 96% PMH: Type II DM, CAD, PVD, HF, A-fib, HTN Lab Values- BNP 466 Na+ 139 K+ 4.3 BUN 25
creatine 1.20 troponin 0.052 CK-MB 2.9. L vent hypertrophy, EF 40/45%, moderate mitral regurg, severe valvular aortic stenosis AAA: MB 64M chest/back pain severe/constant. PMH: HTN
hypercholesterolemia, smoking. ab pain, nausea,T 97.9, BP 90/70, HR 140, RR 24,O2 98% RA tachycardic, Abd: rigid, tender, non-distended. Pulsating palpated in mid-epigastric region; pedal pulses
1+ Aortic Dissection TG 71F hx of AAA, anxiety, leg numbness, severe chest pain, HTN,tachycardia, & nausea; descending & ascending aortic dissection WBC: 2.34, H/H: 6/19, Plt: 126,000, PT/PTT:
35/56,INR: 2.12 pH: 7.12, PaCO2: 45, PaO2: 266, HCO3 15, Lactate: CPK 3000, CPK-MB 35.16, troponin: 42 Ionized Ca: 0.89, K+: 4.2 Aortic Dissection 2- R.S. 46 M. PMH- HTN, DM, obesity, 2 packs/day,
acute onset of tearing/ripping sensation in upper back & chest pain. Diaphoretic BP 199/125, HR 149, RR 30 T 37.7 O2 sat 93% pain 10/10, ↑HR, ↑RR, anxious. Lung crackles, strong murmur in the
aortic valve; pedal & femoral pulses-weak/thready. sinus tachycardia w/ frequent PVCs WBC:3.4;INR:2; HCO3:25; CPK:3000; pH:7.25; Lactate:11; CPK-MB:39; Platelets:12,400; PaCO2:51; Ionized
Ca:0.90; troponin:45; PT/PTT:34/55; PaO2:220; K:5.5 CAD+ Stent Placement: JA 65F, SOB& fatigue. PMH-stroke, taking Coumadin, escalating chest tightness/pain ^HR Peripheral Arterial Disease:KB 68F
frequent severe leg cramping, pain in hips/legs, difficulty being on feet for more than 30 min, toenail-black. Symptoms started 2 mo ago. PMH- diverticulitis, HTN, typeII diabetes,anxiety disorder &
smoking Arteriovenous Malformation- CF 55M playing soccer, collapse, intubated. CT=large ICH (intracranial hemorrhage); can’t open eyes, pupils 2mm/ nonreactive to light; no spontaneous
movement of extremities or spontaneous breathing, elevated cardiac enzymes Kawasaki’s disease: ST 4M, 104.1°F febrile for one wk, not relieved w/ NSAIDS, red, chapped lips & tongue, palms
red/peeling; irritable, lethargic, cervical lymph nodes swollen, autoimmune condition of inflammation of the blood vessels, palmar rash “strawberry tongue.” Beta-Blocker Overdose: 82M weak
pulse,lethargic,LOW BP+pulse, ^lactate, dec.bicarb,EKG-sinus bradycardia Cardiac Tamponade MB, 34F, anxiety, chest pain, breast cancer,radiation ^BP, RR, HR-rub, JVD Hypoten ff Epidural-AW
26, gravida 2 para 1, labor-lactated ringers, hypotension, ephedrine SVC Syndrome JC 30M, edema-up extrem & face, ^vitals except low SPO2, germ cell tumor, pitting edema, jugular venous
distention Retroperitoneal Bleed:RE 53M, chest pain, ST elevation-stents-1 hr later-light-head, back & groin pain, sweaty low BP, Hb, Hct ^^HR, RR Cardioversion:ER 60sF, palpitations, dizzy, sweat,-hx
3 paroxymal atrial fib. eps-^BP, RR, P, BUN (a fib w/rap vent rate) DIC-RS 62M, flu symp, cough, ^T, HR, WBC, PaCO2 low SPO2, pH-resp acid, pneum, decline health, sepsis, cough blood,-low Hb,
Hct, pH, Bicarb, ^^WBC Orthostatic Htn (dehydration)LW 78; syncope hematoma above L eye, low urine O, sinus tachycard, ^ Na, urine osm, BP decrease standing Post Operative Pulmonary
Embolism: (1 KS 22F, scoliosis, shallow breath, P-121,O2-90%,LOW Hgb,Hct, ^D-dimer, pulmonary emboli)(2 EC 46F, obese, hernia mesh replacement, low O2, tightness in chest, breathing hard) (3
SH 65F, total knee replacement, chest discomfort, diaphretic, DVT)(4 SM 77M; inter-trochanteric fracture of L femur; diaphoretic, anxious, tachycardic, bilat LE warm/pink, O2 sat 90%) Pulmonary
HTN: HG 5 moM, respiratory distress, hypoxic, tachypneic, tachycardic, febrile, ^HR RR, low O2 sat., severe nasal flaring/grunting Asthma: ST 4MO; respiratory distress, prolonged expiration, slightly
low O2 sat, wheezing, cough, ^HR RR, low pH, low PaCO2. COPD exacerbation: L.Y. 62F CPAP machine, 76% O2 sat, labor ed breathing, tripoding, tachypneic, anxious, diaphoretic, clubbing, barrel
chest, gray/blue nail beds, ^CO2, low O2, low pH (2 TA 50M gardner, persis cough, SOB, pack/day)(3 SK 60F stress smoker) Emphysema: SH 84M, confusion, lethargy, “grey,” 47% O2 sat, nonbreather; O2 sat 69%, ^RR HR, smoker, barrel chest, ↓temp Cystic fibrosis: HEU 2F, H2Oy/greasy stools for 3 mo, sometimes constipated, malnourished, pale, past coughs; thick grayish mucus, TB: JS
36F cough 2X week non-productive, SOB; exertion/ fatigue, LOA, lost 7lbs in 2 wks, intense PM fevers, traveled, ↑HR, ↑WBC, x-ray; hilar enlargement, consolidation of URL(2-DS 48M; hemoptysis,
fever, night sweats, dull chest pain, HPI: kidney transplant, productive cough)(3-RS 62M; HTN, gout, renal insufficiency; S. Africa) Pediatric Airway Foreign Body: ER 2M, chronic coughing, HR 126, BP
95/52, wheezing, diminished R breath sounds, persistent non-productive cough; Pneumothroax:ES 26M car accident, Lchest wall pain, absent L BS., crepitus, ↑BP,HR(2- LW 22M chest pain, SOB,
appendectomy, ↑BP/HR, BP 129/62, O2 sat 84) Esophageal Leak: CB 58M; lung CA, feeding J-Tube; chronic diarrhea, Klebsiella & C&ida; IBS ARDS TT 53M, dyspnea, PMH:GRED, bilat. inguinal hernia,
vasectomy, lumbar disc surgery, herpes BP 78/48, SaO280% lethargic eventually unresponsive state Interstitial lung disease KP 55M O2sat 55, PMH- HTN, hyperlipidemia sarcoidosis,BUN 40, glu187,
(sinus tachycardia) CXR- low lung consolidation, (2 RJP 68F PaO2 59, PaCO2 30, HCO3- 23 chest x-ray: lungs opaque, tachypneic, labored breathing even on re-breather, ↓FEV1 & FEV, weight loss,
“ABG showed respiratory acidosis” Pulmonary Fibrosis (form of interstitial lung disease)RS 65M wt. loss, dry hackling cough, chest discomfort, & SOB w/ exertion, 30ys coal mines respiratory acidosis
CXR/CT:bilateral reticular & nodular interstitial infiltrates & areas of “honeycombing” Pneumonia CL 14F stomach pain (3 days) head ache, cant tolerate fluids orally, malaise & vertigo w/ position
changes, temp 104.2, crackles noted bibasilar, tenderness in RUQ. Respiratory fail MM 44F; C/O ab pain, N/V, lethargic but oriented, anxious/restless O2-85% BP 88/42, HR 120-sinus tachycardia w/
no ectopy, RR 24 & shallow, oral temp 99.2., BUN & Creatine elevated, CXR showed bibasilar infiltrates Resp fail (2nd to pneumonia) BK 61M right BKA, day 2 post-op, chest tightness, constant nonproductive cough. O2sat 85-88%BP 158/96, HR 118, RR 28 lung sounds had bilateral expiratory wheezing EKG-sinus tachycardia w/ no ectopy CXR- bilateral infiltrates, PaCO2 30, PaO2 51, HCO3- 25
Resp. Syncytial Virus infection EC 6mo (35 weeks premature), rhinorrhea, slight ↑WOB, mild fussiness & pallor, ↓oral intake, tachypnic (RR of 70 breaths per minute) low SpO2, Cyanotic & tachycardic
as temp rises Chest x-ray- mild atelectasis in bilat lower lobes, primary respiratory alkalosis, ↑ WBC Sarcoidosis HM 28F (black), sudden SOB, pressure & tightening of upper chest unaffected by
activity, dry frequent cough,wheezing bilat in upper lobes; lower lobes clear & equal bilat, labs- bilat hilar & mediastonal lymphadenopathy, pulmonary opacities & bronchial wall thickening,
eosinophilia, high erythrocyte sedimentation rate ARF:EC 68F, intra-abdominal abscess, ESBL->klebsiella,low UO,nausea, vomiting (2 post surgical bleed- BK; ab pain (RLQ), N/V, ruptured appendix,
↑BUN/Creatinine AKI: SK 65M black stool x 2 day, weakness, diarrhea, ↓ urine; Hx cirrhosis, htn, tobacco use; lethargic, diaphoretic, pale, abd pain 7/10 ATN:TT 52F, sepsis, BP 60/30, RR 6, HR 55,
cardiopulmonary arrest, low UO, dark amber urine Post-Hemorrhagic Renal Fail 41F, endometrial cancer, 5’4/250lbs, nicked blood vessel during procedure, ARF; ↑BUN, crea; Renal Fail-GI bleed:
MM 39M, hematemesis, melena, 80/40, tachycardic, lethargic, ↑Cr,↓Ca,↑Hgb,↓Hct: Pyelonephritis: SD 31F, 33wks gestation, back pain, preterm contract, N/F, 9/10 L sides flank pain radiated to L
lowab, vom 4x/24hrs, congenital absence R kidney, staphylococcus aureus, WBCs 19.3 (2- BM 29F, C/O bilat flank pain, N/A/C, dysuria, hematuria, urinary frequency, delivered baby 5 days
ago)(3- MR 19; 30 wks gestation, 8/10 ab pain radiates to L flank, C/O ab tightness, UTI: MJE 29F, G1,P0,32wks, dysuria, polyuria (lots of dilute urine), cloudy urine, proteinuria, leukocyte clumps,WBC
esterase; (2- KMM 86F, mental status changes, 146/74, ↑WBC) (3-after repeated catheterizations: EO 20F, sm bowel resection for Crohns, had Foley, unable to void 8 hrs post Foley removal, Foley
over night, removed in morn w/ foul smell, couldn’t void, had urge Hydronephrosis:KP 57M, HTN, DM-II, 10/10 R flank pain, hematuria, ↑WBC/RBC/BUN/creatinine, bacteriuria, kidney stone, UTI
comps Polycystic Kidney Disease:30M, “sharp, crampy” back pain, enlarged kidneys, hematuria, proteinuria (↑BUN/creatinine), renal cysts Renalvascular HTN:EC 3M, L facial palsy, ↑BP, unilateral
renal artery stenosis (means rt kidney producing excessive renin) Utero-Pelvic obstruction: NR 47M, 10K race training for triathalon, L side abd pain, L CVA tenderness, ↑ Cr,BUN. Lrenal obstruction, L
sided CVA tenderness; Acute Tubular Necrosis: TT 52F, sepsis, BP 60/30, RR 6, HR 55; cardiac arrest, 30 mins of resuscitation pt intubated, urine O dark amber color, ↑BUN/ creatinine; Congenital
Nephrotic Syndrome (Finnish Type): KS 1mo(M); respiratory distress, rapid breathing,↓oral intake, fussiness, “puffiness” around eyes, 1 wk runny nose; NICU 1.5 wks: coarse crackles, dimin breath
sounds; ↑BP, 2+ pitting edema, 3+ periorbital edema; ↓Na, ↑K, ↑Cl, ↓Ca, ↓total protein, ↓albumin, ↓serum IgGl ↓creatinine G1,P0,32wks, dysuria, polyuria (lots of dilute urine), cloudy urine, proteinuria,
leukocyte clumps,WBC esterase; (2- KMM 86F, mental status changes, 146/74, ↑WBC) (3-after repeated catheterizations: EO 20F, sm bowel resection for Crohns, had Foley, unable to void 8 hrs post
Foley removal, Foley over night, removed in morn w/ foul smell, couldn’t void, had urge Hydronephrosis:KP 57M, HTN, DM-II, 10/10 R flank pain, hematuria, ↑WBC/RBC/BUN/creatinine, bacteriuria,
kidney stone, UTI comps Polycystic Kidney Disease:30M, “sharp, crampy” back pain, enlarged kidneys, hematuria, proteinuria (↑BUN/creatinine), renal cysts Renalvascular HTN:EC 3M, L facial
palsy, ↑BP, unilateral renal artery stenosis (means rt kidney producing excessive renin) Utero-Pelvic obstruction: NR 47M, 10K race training for triathalon, L side abd pain, L CVA tenderness, ↑ Cr,BUN.
Lrenal obstruction, L sided CVA tenderness; Acute Tubular Necrosis: TT 52F, sepsis, BP 60/30, RR 6, HR 55; cardiac arrest, 30 mins of resuscitation pt intubated, urine O dark amber color, ↑BUN/
creatinine; Congenital Nephrotic Syndrome (Finnish Type): KS 1mo(M); respiratory distress, rapid breathing,↓oral intake, fussiness, “puffiness” around eyes, 1 wk runny nose; NICU 1.5 wks: coarse
crackles, dimin breath sounds; ↑BP, 2+ pitting edema, 3+ periorbital edema; ↓Na, ↑K, ↑Cl, ↓Ca, ↓total protein, ↓albumin, ↓serum IgGl ↓creatinine
Stage 1A
< 20 mm
No nodes
Stage 1B
< 20 mm
Nodal micro.
Stage 11A
< 20 mm
N1
> 20 mm < 50
None
Stage 11B
> 20 mm < 50
N1
> 50 mm
None
Stage 111A
< 50 mm
N2
> 50 mm
N1 or N2
Stage 111B
Chest / skin
N0 – N2
Stage 111C
Any size
N3
Stage IV
Any size
Spread
N0 = no lymph node metastasis | N1 = 1-3 axillary nodes involved
N2 = 4-9 axillary nodes involved | N3 = 10+ axillary nodes involved
Positive feedback causes an LH spike during the ovulatory phase.
The corpus luteum develops during the luteal phase. (HCG maintains)
Ovarian follicle develops into corpus luteum via LH
Progesterone peaks during the luteal phase.
FSH contributes significantly to the follicular phase.
Typically only a single Graafian follicle develops and erupts.
LH peaks during ovulation
Cervix dysplasia in situ: cervical columnar epithelium + vaginal squamous epithelium
Life threatening portal hypertension = esophageal bleed
Jaundice (high blood bilirubin) Ascites (hepatic portal congestion)
Bruises (low clotting factors) Gynecomastia (low steroid clearance)
Vitamin K = clotting factor synthesis in liver | cholera = secretory diarrhea
Conjugation = fat soluble (uncon.) -> water soluble (con) bilirubin
Liver stores B12 for years | B12 is not necessary for platelet maturation.
B12 binds carrier protein transcobalamin -> into tissue.
B12 binds intrinsic factor -> absorbed in the terminal ileum
Thought elaboration + goal oriented behavior = prefrontal
NERNST = 61 * log (K small / K big) | middle cerebral artery = dysphagia