Step 1 Study Cards

Front 1

Muscarinic receptors are found in the _________ and are activated by ______ and blocked by ____________

Back 1

Heart
smooth muscle
glands

activated by ACh and muscarine

blocked by atropine

Front 2

effects of muscarine receptors in the heart, smooth muscle and glands

Back 2

Heart = Ach and muscarine inhibit = decreased HR; conductoin velocity at AV node; decreased contractility --opens K channels in SA node to slow rate of spontaneous phase 4 depol and decrease HR

GI smooth muscle, male sex organs, bronchioles, bladder sphincters = excitatory effects of ACh and muscarine = increased motility and relaxation of sphincters in the gut; constricts bronchiolar smooth muscle; erection; contracts bladder wall; relaxes sphincter - Gq stimulation leading to increased IP3 and intracellular Ca

Front 3

a-1 receptors are excitatory, increase IP3 and Cai via Gq, NE=EPI, and found in ______

Back 3

vascular smooth muscle of skin and sphanchnics (constricts)

Gi and bladder sphincters (constricts)

radial muscle of iris

Front 4

a1 agonists and antagonists

Back 4

NE, phenylephrine = agonists

phenoxybenzamine, phenolamine, prazosin = antagonists

Front 5

a2 agonists and antagonists

Back 5

agonists = clonidine

antagonists = yohimbine

Front 6

B1 agonists and antagonists

Back 6

agonists = NE, Iso, Dobutamine

antagonists = propanolol (nonselective); metoprolol

Front 7

B2 agonists and antagonists

Back 7

agonists = iso, albuterol

antag = propanolol (nonselective), butoxamine

Front 8

B2 and A2 are both ______

A1and B1 both _____

Back 8

inhibitory/relax

have equal sensitivity to Epi and NE and both excite

B receptors via Gs and increased cAMP

a2 decreases cAMP via Gi

A1 increased Cai via Gq, PLC, IP3

Front 9

A2 receptors are found

Back 9

inthe presynaptic nerve terminals, platelyts, fat cells, walls of the GI tract -- relax or dilate -- think decreased GI motility

Front 10

B1 receptors are found

Back 10

AV node, SA node, ventricles of the heart and excite

(have A1 too, but B1 receptors more sensitive to Epi and NE than A1 so they dominate here)

Front 11

B2 receptors are gound where?

Back 11

vascular msooth muscle of skeletal muscle (dilates)

bronhcial msooth muscle (dilates)

walls of GI, GU, Bladder
- dilates bladder wall and decreases GI motility

Front 12

uterine contraction is mediated via ______

uterine relaxation is mediated via ________

if all B receptors are blocked, then Epi acts as ______

Back 12

a1

B2

an alpha agonists --- increases uterine contraction

Front 13

phosphorylation of MLCK has what effect on smooth muscle?

Back 13

relaxation
(think increased cAMP and activation of PKA -- done via B2 receptors)

Front 14

activation of MLCK is done via what receptor?

Back 14

a1 (via increased PLC and increased IP3 via Gq OR decreased cAMP and decreased PKA activity resulting in non-phosphorylation of MLCK) -- MLCK active -- contration of smooth muscle

Front 15

Epi has higher affinity for ______ than __________

Back 15

B receptors over A receptors so you see B effects first

Front 16

PAS staining - stains red/pink for _______

Back 16

polysacc
glycoproteins

zona pellucida = ex

Front 17

inadequate oxygenation of tissue

sx associated?

causes

Back 17

hypoxia

cyanosis (<80% SaO2), confusion, cognitive impairment, lethargy

causes =
ischemia

hypoxemia (low PaO2)
ventilation defect (perfused but not ventilated - intrapulmonary shunt)

perfusion defect (ventilated but not perfused - dead space)

diffusion defect (interstitial fibrosis, pulmonary edema)

Hb abnormalities (anemia, methemoglobin)

Front 18

falsely high oxygen saturation on pulse oximetry is due to?

Back 18

methemoglobin
carboxy hemoglobin
usually, these decrease oxygen saturation but cannot be detected by this method so oxygen saturation appears high when it is not -- use co-oximeter to avoid this

Front 19

define ischemia

examples?
consequences?

Back 19

decreased arterial blood inflow or venous outflow of blood

ex: coronary artery atherosclerosis, decrased CO, thromosis of splenic vein

consequences are atrophy, infarction (localized necrosis), organ dysfunctoin (heart failure)

Front 20

driving force for O2 to go from capillaries to tissue is ______

determined by ______

causes for reduction?

Back 20

PaO2 (keeps O2 dissolved in blood)

atmostpheric oxygen, exchange level at the lungs

hypoxemia - decreased inspiration (high altitude)
hypoventilation due to respiratory acidosis
increased alveolar PCO2 (always causes a decrease in PaO2)

Front 21

what is SaO2? what is it determined by? determining factors?

Back 21

% oxygen saturation (% of Hb that are bound by oxygen)

determined by:
heme valence - O2 can't bind to Fe3+
PaO2 levels determine this - if low, SaO2 will also be low b/c less O2 available

Front 22

total amount of oxygen carried in the blood is determined by?

Back 22

Hb concentration in RBCs (most sig - determines amount delivered to tissue), PaO2, SaO2

Front 23

causes of anemia

does PaO2 change? SaO2?

Back 23

defintion = decreased Hb concentration (7g/dL)

1. decreased production of Hb - iron deficiency
2. increased destruction of RBC - hereditary spherocytosis
3. decreased prodcution of RBCs - aplastic anemia
inc sequestration of RBC - splenomegaly

arterial oxygen pressure does not change - determined by ventilation and atmospheric pressure

saturation of oxygen does not change - the Hb that is there is still with the same binding capacity

Front 24

oxygen binding curve logistics:

decrease O2 affinity means less O2 to tissue - curve shifts ?

Back 24

to the right to decrease O2 affintity
(think - decreased affinity means increased H+, BPG, temperature, altitude)

likewise - decreased BPG, H+, tempterature, and altitude shift the curve to the left or toward Hb with higher affinity

increased O2 affinity means increased O2 saturatoin

Front 25

What is met hemoglobin

Back 25

ferric heme (+3)
converted to +2/O2 binding state via NADH
occurs with newborns when deficient in cyochrome b5 reductase which is the enzyme for this process = congenital def

also occurs with nitrite drugs, sulfa drugs, sepsis, local anesthetics

decreased o2 saturatoin

Front 26

chocolate blood

Back 26

methemoglobin (+3)
tx = IV methylene blue - acts as a reduced electron carrier in the PPP

Front 27

normal PaO2
decreased SaO2

Back 27

CO poisoning (tx = 100% oxygen)
methemoglobin (tx = IV methylene blue)

both left shift the oxygen binding curve to compensate and increase the SaO2

Front 28

hypoxemia fixed with pure oxygen

Back 28

dx = perfusion defect (ventilated but not perfused - other areas supplement loss)

ventilation defect -- no change

Front 29

cherry red discoloration of skin and blood
lactic acidosis
hypoxia
decreased oxygen saturation

Back 29

CO poisoning - leading cause of poisoning

think inhibition of cytochrome oxidase in the ETC

Front 30

inhibit cytochrome oxidase

Back 30

CO
CN

think - decreased ATP production due to disruption of H+ gradient

think house fires

Front 31

tx of CN poisoning

Back 31

amyl nitrite
thisoulfate

Front 32

uncouplers of oxidative phosphorylation that don't damage the inner mitoch membrane - destroy the gradient only

common sx?

Back 32

DNP
thermogenin (brown fat - newborn)
alcohol
salicylates

hyperthermia

Front 33

tissues most susceptible to hypoxia

Back 33

watershed areas between major arteries (b/w ACA and MCA; sup and inf mesenteric)

subendocardial tissue (ischemia here results in chest pain and ST segment depression on ECG -- due to coronary artery athero; also caused by increaed demand on LVH heart)

renal cortex and medulla (straight prox tubule and thick asc limb respectively)

neruons

zone III hepatocytes around central vein

Front 34

consequences of hypoxic cell injury

Back 34

decreased ATP synthesis
anaerobic glycolysis -- lactic acidosis
impaired NaK atpase - sodium and water into cell and swelling

decreased protein synth (ribosomes can't attach)

impaired Ca ATP pump (so Ca floods cell - enzymes activated - endonucleases activated -- fading of nuc = karyolysis)

CA in the mitoch cause apoptosis via cytochrome c activtion in cytosol

Ca into cell = point of no return

Front 35

most detructive free radicals

FR function?

Back 35

hydroxyl free radicals (think H202 and ionizing radiation - Fe and Cu)

FRs damage DNA and membranes (increased Ca into cell)

Front 36

free radical formation related to drug toxicity

Back 36

acetomenophen - liver

Front 37

best neutralizer of hydroxyl radical?

neutralizer of acetomenophen, hypdrogen proxide, hydroxyl FRs?

Back 37

vitamin C

glutathione peroxide (N-acetylcysteine = GSH or glutathione increases as are result)

others = vitamin E (think LDLs and fatty streaks) and SOD

Front 38

mechanism of ischemia reperfusion injury in acute MI

Back 38

superoxide FRs and cytosolic Ca irreversibly damage previously injured cells upon restoration of blood flow

Front 39

think cytochrome c ....think

Back 39

mitochondrial release
activates caspases to initiate apoptosis

elicited by etoh, salicylates, increaed cytosolic Ca

Front 40

SER hyperplasia due to _______
causes?

SER inhibition is caused by? effects?

Back 40

induction of CYP450

increases drug metabolism

think etoh, barbs, phenytoin

SER inhibition
caused by proton receptor blockers, macrolides, histamine blockers, resulting in decreased drug metab

Front 41

defect in post-translational modificatoin of lysosomal enzymes -- results in empty lysozomes (lack of enzyme targeting by mannose phosphorylation) and undigested substrates accumulate in the cytosol which contain carbs, lipids, and proteins

sx = psychomotor retardation and early death

Back 41

inclusion (I) cell disease

think phophotransferase (for mannose) deficiency

Front 42

microtubule dysfunction and/or enzyme lysosomal enzyme dysfunction in immune cells (PMNs, leukocytes, etc) can result in susceptibility to what kind of infection?

AR disease that displays this due to defection in phagolysosomal formation?

Back 42

bacterial

chediak hagashi syndrome
staph aureus and other bacterial infections are common

Front 43

defects in synthesis of tubulin in the G2 phase of the cell cycle

Back 43

etoposide
bleomycin B

Front 44

drugs that attach to tubulin of microtubules and interfere the production of the mitotic spindle

Back 44

vinca alkaloids
colchicine (gout)

Front 45

drug that enhances tubulin polymerization and thus interferes with disassembly of the mitotic spindle

Back 45

paclitaxel

Front 46

mallory bodies

Back 46

ubiquinated intermediate filaments targeted for degradation in the cytoplasm -- eosinophilic -- asociated with hepatocytes and alocholic liver dz

Front 47

_______ targets intermediate filaments for degradation

inclusions it forms?

Back 47

ubiquitin

mallory bodies in hepatocyes

lewy bodies in damaged neurofilaments of parkinson's in disentigtrating substantia nigra

Front 48

accumulation of unconjugated bilirubin in the cell causes what sx

Back 48

kinicteris (remember Bu is fat soluble) -- associ with Rh hemoltyic dz of newborn -- can enter basal ganglia of brain and cause permanent damage

Front 49

accum of cholesterol inside cell causes what sx?

Back 49

xanthelasma -- yellow plaque on eye -- seen in mphages

accum insmooth muscle and mphages (foam cells) = components of fibrofatty plaque in atherosclerosis

Front 50

accum of glycogen in the cell is assoc with?

Back 50

DM (prox renal tubule cells - insensitive to insulin so overload with glycogen)

von gierke's glycogenosis = glc 6 phosphatase deficiency -- excess in renal tubule cells and hepatocytes

Front 51

melanin deposition in skin and mucosal membranes associated with?

Back 51

increased ACTH (stimulates melanocytes)

seen in Addison's dz (adrenal cortex destruction)

Front 52

intracellular accumulation of protein seen in what dz

Back 52

amyloid

Front 53

fatty liver dz has accum of what in the cytosol?

Back 53

TGs - packed VLDLs

mcc cause is etoh