BHS 116.3- Physiology III
Notetaker: Vivien Yip
Date: 5/1/13
Page: 1
Not all inclusive
- Approximately 70 questions
- About 60-65% new material
- About 20% from exams 1 & 2 on immunology (lecture 18 on vaccines will not be included)
- About 10% from exam 3 on primarily renal with some reproductive physiology
- 4-5 questions from presentation handouts (1 from each topic and maybe a 2 nd question from one of
them)
Final Exam Review
Inflammation
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cardinal signs: what they are, what do they mean
acute and chronic: differences, cellular mechanisms
innate immune system
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physical barriers to infection: epithelial barrier (skin), mucus, saliva, tears
phagocytic cells: macrophages, neutrophils
NK cells: cytotoxicity
Complement system: MAC
Cytokines and plasma proteins: interferons, CRP
Fever
know major differences between innate vs adaptive
adaptive immune system
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antigen recognition molecules
more specific type of immunity, longer lasting, greater degree of diversity
b cell, t cell
complement system
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major system involved in attacking primarily bacteria and ab/ag complexes
main complement protein: tend to get broken into a and b component
“b” are opsonins, bind to membranes
“a” act as cytokines to draw more leukocytes to the site, increase inflammatory response
complement activation pathways
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leads to formation of MAC, poke holes in target (bacteria or another type of cell) and kill that cell
specific sequence involved in making those MAC, 3 pathways: alternative, classical, lectin
pathways
alternative: most different
classical and lectin: pretty much identical all the way through w/ exception of initiation
C1- classical, manose binding lectin – initiates lectin pathway
antibodies
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structure: 2 HC & 2LC
both LC will be the same group
gamma, delta, miu HC
function: different isotypes, class switching
distinct regions: variable will serve as antigen binding sites
BHS 116.3- Physiology III
Notetaker: Vivien Yip
-
Date: 5/1/13
Page: 2
constant: structural in nature
lymphocyte maturation
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B cell goes through specific maturation process, different from T cell maturation process
B cell: express both IgM and IgD on surface in order to get full mature B cell
all this is occurring in bone marrow for B cell
T cell maturation process occurs in thymus
once each of these reach maturity, it can leave its primary lymphocytic organ and migrate to
lymph node, spleen, MALT (secondary lymph organ) where it encounters Ag for the first time
T cell subsets
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cytotoxic CD8+
helper CD4+
all T cells will have CD3+
Can further subdivide helper T cells into Th1 (primary helper T cell) and Th2 (found more in
parasitic type infection)
T cell activation CD4+
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2 signals required
first: MHC binding to T cell receptor
second: CD8 of T cell binding to b7 on the APC
then IL2 released can bind to IL2 receptor and trigger proliferation of T cell
CD8+ activation
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infected cell that is phagocytosed by APC
o expression of MHC I and MHC II
initial signal: CD8+ binding to MHC I on APC
CD4+ binding to MHC II
o release cytokines, act as second signal for that CD8+ T cell
o proliferate and activated
other form is standard: MHC T cell receptor complex, followed by CD8 b7 complex
effector function of CD4+ T cell
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activating macrophages, many times they will phagocytose microbes but won’t be able to kill it
CD4+ will help stimulate that process and allow it to kill the phagocytosed microbe
activate and provide second signal for B cells – lead to class switching of antibody
Ig Class change
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only B cell activated by CD4 + T cell can class switch their type of antibody
IgM is initial class
if CD4+ T cell help, will allow for different isotypes
effector function of CD8+ T cell
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directly kill infected target cell
stimulate lysis reaction and trigger apoptosis of infected cell
primary vs secondary antibody responses
BHS 116.3- Physiology III
Notetaker: Vivien Yip
-
Date: 5/1/13
Page: 3
primary: frist time exposure to antigen, slower rxn, not very high stimulus, produce IgM, pool of
memory cell against the antigen, if we encounter again, will get secondary response
secondary response: greater, faster and produce IgG
B cell activation
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T cell dependent (protein antigens), with CD4 help
o CD4 can only present protein peptides to MHC to be recognized
o utilize helper T cells to further stimulate activated B cell
o provides 2nd signal for antibody class switch
T cell independent (non protein antigens)
o carbohydrates, nucleic acids, some instances lipids
o does not utilize helper T cells to further stimulate B cell, no 2nd signal provided and no
antibody class switch
o weaker response
o produce only IgM (secretory)
Transplantation
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4 types: allogenic, xenogenic, autograft, isograft
mechanism of rejection
hypersensitivities
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4 primary types:
1: immediate, IgE mediated
2: IgM, IgG mediated, against a tissue antigen
3: immune complex, IgM or IgG bound to soluble antigen forming complex that triggers
inflammation
4: only T cell mediated hypersensitivity reaction
autoimmune diseases
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classify according to:
o systemic/organ specific
o antibody mediated t cell mediated or both
o mechanism: type of hypersensitivity rxn
o MG, SLE, Scleroderma, Sjogren’s, Graves disease, Multiple sclerosis, Type I diabetes,
Rheumatoid Arthritis, Hashimoto’s thyroiditis
Urine Function
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general process of urine formation
filtration, reabsorption, secretion and combination of those 3 leads to amount of specific solute
that is excreted in the urine
GFR
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hydrostatic, colloid osmotic forces both in glomerulus and bowman’s capsule
how those things change w/ compression of afferent and efferent arteriole or dilation
autoregulation of GFR and renal blood flow
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myogenic
BHS 116.3- Physiology III
Notetaker: Vivien Yip
-
Date: 5/1/13
Page: 4
o both arterioles have smooth muscle
o afferent has normal response to stretch
o increase or decrease amount of blood flow in glomerulus
tubuloglomerular feedback
o JG cell and macula densa (MD)
o depending on NaCl concentration in distal tubule that gets to MD
o MD have chemoreceptors that sense NaCl, trigger JG cells to release renin there’s when
low levels of NaCl
Peritubular capillary and renal interstitial fluid physical forces
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Pc, opposes capillary reabsorption
Pif, favors capillary reabsorption
πif favors capillary reabsorption
πif opposes capillary reabsorption
Proximal tubules
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2/3 of everything getting reabsorbed
other regions have specific things going on, know what is absorbed or secreted
o distal tubule and cortical collecting tubules
 principal cells: reabsorption of Na and by default water, secrete K+ back into
renal tubules if we have too much K+ in blood
 intercalated cells: reabsorb bicarbonate and K+, secrete H+ (acidic condition)
Aldosterone
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direct effect on principal cells: increases Na+ reabsorption and K+ secretion
Osmoreceptor ADH feedback
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role in different osmolarities in blood
high osmolarity in blood: want to reabsorb water to dilute, release ADH, acts on late distal tubule
and cortical collecting tubules
Summary of urine excretion
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late distal tubule and collecting tubule are sensitive to ADH
in the presence of ADH they will reabsorb water and produce a concentrated urine
early distal tubule and thick ascending limb are always impermeable to water no matter what,
reason why it’s called diluting segment
absence of ADH, whole back end is impermeable to water  get very dilute urine, not
reabsorbing any water
renal potassium excretion
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greatest variation is due to secretion of potassium back in by principal cells
calcium and phosphate handling
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Ca++ majority is reabsorbed in proximal tubules, another area is in later portion of renal tubules
o early distal or late distal (under PTH control  will reabsorb if present)
P, mostly reabsorbed along length of proximal tubule, in the presence of PTH the reabsorption is
inhibited
BHS 116.3- Physiology III
Notetaker: Vivien Yip
o
Date: 5/1/13
Page: 5
PTH  phosphate is excreted more
Acid base regulation
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fundamental mechanisms in which kidneys regulate ECF H+ conc:
o secrete H+
o reabsorb filtered bicarbonate
o production of new bicarbonate
primary mechanism will be in proximal tubule: h+ secretion and bicarb reabsorption go hand in
hand  indirect reabsorption
o not reabsorbing the filtered bicarbonate, processing it in epithelial cell and reabsorbing
the newly created bicarbonate, getting 1:1 but not getting the same exact one that was
filtered
In early portion of tubules, we have Na+/H+ counter transport – secondary active, Na+ goes into
renal epithelial cell, H+ is pumped out
o get one bicarbonate reabsorbed
Latter part of tubules: primary active transport of H+, if bicarb still remaining in tubules, will get
indirect reabsorption
o can get phosphate and create new bicarb
in times of acidosis, will get more of the ammonia system playing a role, create a lot more
bicarbonate when we involve ammonia system, kicks in only with acidotic conditions in the
blood
Renal clearance
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Primary renal filtration rate is 125ml/minute
what value means it is filtered reabsorbed or secreted
= inulin, filtered not reabsorbed, not secreted
<inulin, filtered, reabsorbed, secreted
>inulin, filtered, not reabsorbed, secreted
renal pathologies
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acute vs chronic
primary acute type: acute glomerulonephritis
2 primary mechanisms, both involving autoimmunity
o circulating immune complexes embedded in subepithelial or subendothelial tissue,
complexes trigger inflammatory response
o antibody binding to glomerular tissue: in capillary or basement membrane, trigger
inflammatory reaction
o know type II or III hypersensitivity rxn
acute tublar necrosis
o ischemic form: decreased oxygen delivered to renal epithelial cell, can get necrosis, focal
type, sporadic, regions of necrosis and then regions of normal cell, form casts of necrotic
debris that plug up tubules downstream
o nephrotoxic: due to poisons, long regions of necrosis, plug up regions downstream
chronic glomerular nephritis
o if the offending agent is still around from acute glomerular nephritis
o irreversible damage to nephron
chronic obstructive pyelonephritis
o usually superior and inferior poles of kidneys are destroyed
o caused by UTI
BHS 116.3- Physiology III
Notetaker: Vivien Yip
abnormal nephron function
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due to loss of nephrons that is irreversible
loss of water and electrolyte balance
decreased waste product excretion
uremia
anemia
osteomalacia
Date: 5/1/13
Page: 6