Test 1: Adair - Muscle
Na+ channel selectivity filter  glutamate
Permeability of molecules w/o protein channels: nitrogen > water > urea > glucose > ions >
albumin
Review hypertonic, hyperosmotic
Low serum K+: EK more negative, Vm more negative
6 mo endurance exercise training: all increase mt content, oxidative enzymes, capillary density,
myoglobin content… and fiber diameter does not increase
Most likely in increase velocity of shortening: longer muscle, decreased afterload
Myasthenia Gravis: damage to acetylcholine receptor, post-synaptic
Lambert-Eaton: damage to calcium channel, pre-synaptic
Mechanism of Ca++ release from terminal cisternae: Ca-activated in heart, voltage activated in
skeletal muscle
General anesthesia, muscle rigidity, high temp: decreased calcium binding to calsequestrin
Length tension diagram: Active = total – passive
Total is line at very top, passive starts low and increases
Normal Sk. Muscle contraction
1. Activation of dihydropyridine voltage sensor
2. Activation of ryanodine receptor
3. Ca++ release from terminal cisternae
4. Increased Ca++ conc. In sarcoplasm
Excitation-contraction coupling in sm. Muscle: Myosin based, Ca++ binds calmodulin
HEENT exam
Type I sk muscle fibers: increased mt content (Know other comparison w/ type II)
Malignant hyperthermia  genetic disorder
Block 2: Wilson - Hematology
Low Hb, low Hct, low epo  kidney failure
Hx of smoking High hct, normal WBC, normal platelet, slightly increased Epo  secondary
polycythemia
Iron uptake from small bowel mediated by: transferrin receptors on intestinal epit cells
Phagocytic in tissues, sends early signals to initiate inflammatory response: macrophages
Adhesion of neutrophils to inflamed epit: selectins and integrins
Possible ruptured appendix, increase WBC count: due to mobilization of mature neutrophils
from BM
Peripheral smear shows numerous blasts and large # abnormal immature w/ incompletely
segmented nuclei w/ few granules  acute myeloid lymphoma
Allergic rxn  cross-linking of IgE receptors
CD8+ interacts w/ MHC Class I
Helper T direct their own cellular proliferation as well as proliferation of other immune cells
Type A needs packed RBCs: can use type A or O
Woman is A-Rh neg, Child O-Rh positive. Child is anemic and very high bilirubin  Tx. repeated
exchange transfusion w/ O-Rh neg blood
IV drug user, chronic hep C, intractable nosebleed, INR is 7.0  Tx. Fresh frozen plasma
Hx of excessive bleeding, often bleeding into joints, genetic  inherited through mother
Heparin prevents blood clotting via binding and potentiating anti-thrombin III
Severe but undiagnosed gluten sensitivity w/ diarrhea and weight loss, excessive bleeding w/
markedly prolonged prothrombin time 37s  vitamin K deficiency
Sepsis, persistent bleeding from gums, around IV catheters, WBC is high w/ normal
morphology, few immature neutrophils, reduced platelet count  disseminated intravascular
coagulation
Predominant WBC in circulation = neutrophils
DiGeorge Syndrome causes absent thymus  impaired humoral and cellular immunity
Intestinal hookworms, cell type likely increased  eosinophils
Xenograft likely to be associated w/ what type of organ rejection? Hyper-acute or acute
Hemophilia A and B affect which pathway of blood coagulation? Intrinsic pathway only
Block 3: Chade/Granger – Cardio
Preload in ventricular PV graph  point C/ end diastolic pressure
PV diagram systole: C to A
Atrial contraction may contribute up to 25% of ventricular filling
AP arrives at AV bundle: 0.12 seconds
Phase of ventricular muscle AP has highest K+ permeability: 3
Results in dilated heart: decreased Ca++ ions in blood
Ach causes hyperpolarization of SA node
Counting HR from EKG
Einthoven’s Law: I + III = II
aVR in EKG, positive terminal  right arm
ventricular depolarization wave -60° in frontal plane causes large negative in lead III
purkinje fiber rate: 15-40
AP reaches ventricular septum at 0.16 seconds
Sympathetic stimulation of heart releases norepi at sympathetic endings
Know how to calculate mean electrical axis
Know current of injury to determine location of injury/infarct
EKG: paroxysmal ventricular tachycardia, Afib
Circus mov’ts leads to vfib. Increases tendency: decreased conduction velocity, decreased
refractory period, high extracellular K+, longer conduction pathway
Afib  rate of ventricular contraction is irregular and fast
Inverted P wave AFTER qrs complex = premature contraction originating low in AV junction
Systolic-diastolic murmur = PDA
Patient in shock from blood loss  give whole blood
Systolic murmur, QRS axis -30°  aortic stenosis
Diastolic murmur, pulmonary congestion  mitral valve stenosis
Second heart sound assoc w/ closing of pulmonary valve
Digitalis inhibits Na/K pump, increases intracellular Na+ and decreases Ca++ efflux
Standing up from supine: Inc mean circulatory filling pressure, strength of contraction, dec
parasym nerve activity
Exercise: inc arteriole diameter, adenosine conc and dec in resistance
Response to inc arteriole diameter: dec vascular resistance, inc capillary hydrostatic P & lymph
flow
Aortic valve stenosis: dec pulse pressure, stroke volume and systolic pressure
Renovascular hypertension: Inc TPR, ANG II and dec in RBF
Constriction of carotid artery: dec nerve impulses from carotid sinus, inc SV and filling pressure
CHF: inc venous hydrostatic P, capillary hydrostatic P, interstitial fluid V
O2 consumption, CO, pulmonary O2 conc calculation
RVR calculation
NOT responsible for increase in SV in response to inc venous return: decreased left atrial P
Due to stretch of r atrium (Bainbridge reflex), stretch of SA node, Frank-Starling,
increased r atrial pressure
Increased resistance to venous return would decrease CO
Most likely cause of cardiac pain from acute ischemia  lactic acid
Increase coronary BF: dec resistance, inc adenosine, vascular conductance, workload
Substances in plasma that contributes LEAST to plasma colloid osmotic P: chloride
Increased cerebral BF due to inc tissue hydrogen ion conc
Administration of ACE inhibitor: inc Ang I, bradykinin and RBF
Increase in diameter leads to increase in vascular conductance
Which would lead to increase net mov’t Cl- across capillary: inc in conc. Diff of ClPrimary hyperaldosteronism hypertension: inc ECF volume, dec renin and plasma K+
Most likely cause of obesity related increase in BP  inc sympathetic activity
Which Na+ intake will have greatest reduction in BP in response to ACE inhibitor: lowest amt
Response to reduction in arterial pressure  decreased vascular resistance since BF is constant
Greatest flow: high radius, low viscosity
Changes in plasma conc expected to cause greatest activation of chemoreceptor reflex:
Dec O2, inc CO2 and H+
Best drug for angina: nitroglycerin
Decrease in which is most likely explanation of high pulse pressure? Arterial compliance
Occurs in response to elevated atrial P: dec renal sympathetic N activity, inc ANP, Na+ excretion
J point: entire ventricle is depolarized
2nd degree AV block – Mobitz I…
Cardiac reserve is always reduced in cardiac failure
Associated w/ decreased CO: hypothyroidism
Decreased CO, decreased BP, inc HR, inc right atrial P: increase in lymph flow in lower
extremities expected
Decrease in arteriole diameter in local tissues: dec interstitial hydrostatic P, capillary
hydrostatic P, lymph flow and blood flow
What is correct about cardia afterload: it is the resisting force on ventricular wall during systolic
ejection
AV node is site where impulse is delayed the most
QT interval represents: depolarization and repolarization of ventricles
Block 4: Hall - Renal
Decrease in afferent resistance: increase glomerular hydrostatic pressure, increase GFR,
increase RBF
Primary aldosterone: dec plasma K+, inc plasma pH, decrease renin, inc BP
Which increases peritubular capillary reabsorption: inc peritubular capillary colloid osmotic P
Liddle syndrome: dec plasma renin , plasma aldosterone
Inc BP and no change in Na+ excretion
Reduced efferent arteriole resistance: inc RBF, peritubular capillary hydrostatic P
Dec GFR and glomerular capillary hydrostatic P
Large decrease in plasma protein conc tends to cause all except: inc BV
SIADH effect on intra and extracellular fluid: increase both volumes, decrease both osmolarities
Osmolarity calculation. Glucose completely metabolized, just changing total volume
BW = 50 kg
Plasma Na+ conc. = 160 mmol/L
Plasma osmolarity = 340
ICF = 40% and ECF = 20%
Adding 2.0L of glucose  ECF osmolarity = 319 mOsm/L and ICF V = 21.3 L
Runner loses 3L from sweating, drinks 3 L water. Which changes would you expect?
Inc Intracellular V, dec intracellular osmolarity
Dec extracellular V and osmolarity
Greatest decrease in GFR = 30% increase in afferent arteriolar resistance
Decrease efferent resistance: increase RBF, decrease GFR and FF
Reduction in proximal tubule NaCl reabsorption: dec GFR, inc afferent resistance, dec RBF
Bicarb in the urine is normally higher than in glomerular filtrate
FF = GFR/RBF
Dehydrated person w/ severe central diabetes insipidus w/ no ADH, where is osmolarity
lowest? Fluid leaving collecting duct/urine
GFR reduced to 50% normal: no change creatinine excretion rate, decreased clearance,
increased plasma creatinine
Type A intercalated cells: secretion of H+, reabsorption of HCO3- and reabsorption of K+
Transport maximum calculation
Rate of potassium excretion calculation (make sure you convert from L to mL)
Clearance calculation using PAH to get RBF
Free water clearance: urine flow – (U osmolarity x U flow)/Plasma osmolarity
Primary aldosteronism: NC K+ excretion rate, Na+ excretion rate, inc plasma pH, dec plasma K+
conc, inc BP
Greatest impairment of urine concentrating ability  chronic tx w/ furosemide
ADH does NOT increase urea reabsorption by cortical collecting tubule
ADH activates UT-A1 and UT-A3 in collecting ducts
UT-A2 facilitates passive diffusion of urea into thin loops of Henle
Salt-sensitivity of BP would be increased by: loss of fxnal nephrons due to CKD, inability to
suppress Ang II, primary aldosteronism, Tx w/ an ACE inhibitor
Know what causes K+ to move into and out of cells
Person increases K+ intake: Inc K+ excretion, NC in Na+ excretion, inc plasma K+ by < 1mmol/L,
inc aldosterone
Aldosterone antagonists do NOT cause hypokalemia
Carbonic anhydrase inhibitors tend to cause metabolic acidosis
Thiazide diuretics inhibit Na-Cl cotransporters in distal tubules
Osmotic diuretics increase K+ secretion
Na+ channel blockers/amiloride block transport across luminal membrane of collecting
tubules
Loop diuretics tend to cause hypokalemia
Chronic nephrogenic diabetes insipidus: inc urine V, dec urine osmolarity, inc free water
clearance, dec renal medullary osmolarity
Acidosis: inc. urine NH4+ excretion, new renal bicarb
Dec urine excretion bicarb, urine pH
Block 5: Hester - Respiratory
PaO2 equation
Venous blood in anemic person  lower O2 sat and content
O2 consumption equation
Increase in Zone 1 conditions: positive pressure ventilation
Cheyne Stokes Respiration: disordered breathing resulting from instability of resp control sys
Increase airway resistance: activation of parasym nerves
*Aspirated foreign body in right main bronchus  BF decreases
Day 1 after being in space: increased urinary output
Blocking airway leads to increase in Zone 1
COPD, low PaO2, cause of edema: R ventricular failiure due to hypoxic pulmonary hypertension
Low arterial O2, increased PCO2: increased carotid body impulses and inc ventilation rate
Lung capacities and volumes
O2 content and saturation calculations
Inspired O2 lower than 21% = decrease in H+ ions at central chemoreceptors
Beta adrenergic causes decrease in airway resistance
Alveolar Ventilation and minute ventilation equations
Pulmonary HTN, most likely cause of inc pulmonary vascular resistance  decreased PAO2
Increase in HR due to mild exercise and doubling CO, what is change in PA pressure: 5 mmHg
Not important in O2 delivery w/n exercising muscle: decreased H+ conc
Respiratory distress of newborn: decreased compliance, inc surface tension
Highest velocity of flow in lung  right after start of inhalation
Largest pressure differential b/t alveolar P and pleural P: at end of inhalation
Arterial content calculation
Does NOT cause airway narrowing in asthma attack: destruction of airways
Normal V/Q ratio of 0.8: P02 = 100 and PCO2 = 40
V/Q ratio of 0: PO2 = 40 and PCO2 = 45
Most likely pleural effusion in which circumstance? Infection of pleural space destroying
capillary membranes
Block 6: Adair - GI
Cell types and GI proteins they secrete
GLIP stimulated by lipids, carbs and polypeptides
Increase in spike potentials  parasym stimulation
Achalasia  megaesophagus
Decrease in salivary flow from parotid gland: fear
Increased by: smooth objects, nausea, chewing, taste/smell
Pernicious anemia caused by untreated atrophic gastritis
Secretagogues for gastric acid under normal physiological conditions: Ach, histamine, gastrin
Gastric acid secretion in response to meal
1. Increase in pH of gastric contents
2. Increase in rate of acid secretion
3. Decrease in pH of gastric contents
4. Decrease in rate of acid secretion
Severe diarrhea by opening Cl- channels  chorea toxin
Fructose is not disaccharide
Know disaccharides
Assimilation of fat
1. Emulsification of fat
2. Micelle formation
3. Absorption of fat by enterocytes
4. Secretion of chylomicrons
Causes voracious feeding and obesity: lesion that damages VM nuclei of hypothalamus
*Urinary nitrogen excretion calculation
RQ for untreated diabetes = 0.7
H. pylori causes damage via NH4+
Block 7: Ryan – Endocrine
Hormone receptor types: IGF-1 uses enzyme linked receptor
Increased fasting insulin, high FFA, high IGF-1: Inc. GH somatostatin gluconeogenesis, Dec GHRH
total body fat mass
Adenoma secreting GH and TSH: dec GHRH, inc GH IGF-1 TSH T3/T4
Increase in ECF osmolarity increases ADH
GH most likely to exhibit nocturnal peak
Pregnancy can result in euthyroid even though total T3/T4 are high
Fxn of T3: increases gluconeogenesis, glycogenolysis, lipolysis, decreased serum cholesterol
Chronic untreated hypoadrenalism: Dec BP, ECF volume, cellular pH
Inc plasma K+ and no change in urinary Na+
Conn’s syndrome/primary aldosteronism: high ECF volume
Vitamins for fetal physiology
Vitamin D  bone growth
Vit K  liver production of prothrombin
Vit C  bone matrix
Vit E  early embryonic development