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Pathophysiology > TC5 > Flashcards

TC5 Flashcards

1
Q

what does acidemia increase or decrease excretion of? what are the mechanisms?

what about for alkalemia?

A

acidemia: lowers urinary HCO3 excretion, increase urinary NH4 and decrease Titratable acid excretion

it increases NH4+ secretion by increasing glutamate uptake + pathway, and stimulates NH4+/Na+ exchange and H-ATPase activity

Alkalemia increases hco3 excretion, decrease H+ secretion (so low that can’t reabsorb hco3 as much), and decrease NH4+ secretion. net acid secretion (NAE) = 0

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2
Q

how does hypochloremia (from NG suction or vomiting or excessive diuretic use) affect net acid excretion?

A

hypochloremia causes metabolic alkalosis and hypokalemia (same as hyperaldosteronism)

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3
Q

what is the mechanism by which changes in plasma K+ concentration affects net acid excretion, causing metabolic alkalosis or acidosis?

A

hyperkalemia increases + charge in lumen so less H+ secretion. also decreases NH4+ production and secretion so less HCO3- is reabsorbed

hypokalemia is just opposite

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4
Q

equation for urinary net acid excretion NAE

A

NAE = (mEq NH4+ + mEq H2PO4- - mEq HCO3-) x liters of urine per day

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5
Q

which stimulator is most potent for meal stimulated acid secretion?

A

gastrin -> increase histamine release-> stimulate parietal cells (H2 receptor)

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6
Q

what is responsible for cephalic phase of acid secretion in stomach?

what about gastric phase?

intestinal phase?

A

cephalic phase: vagal nerve/ ACh

gastric phase (biggest one): chemical products of digestion and gastric distention -> increase gastrin secretion and vagal activity

intestinal phase: duodenal peptides stimulate gastrin secretion of duodenal G cells

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7
Q

name the 5 cells in oxyntic glands and what they secrete

A 
parietal cell - IF and HCl
ECL - histamine
enterochromaffin - ANP
D cell - somatostatin
chief cell - pepsinogen and leptin
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8
Q

what are the 4 phenotypes of chronic gastritis from H. pylori infection? effect on HCl secretion, and what they’re at increased risk for?

btw they all start from the antrum

A
  1. nonatrophic pangastritis.
    little effect on HCl
    may acquire gastric MALT lymphoma
  2. antral predominant gastritis
    increased HCl
    risk for duodenal PUD
  3. corpus predominant atrophic gastritis
    decreased HCl
    risk for gastric PUD and eventually gastric adenocarcinoma
  4. multifocal atrophic pangastritis
    hypo or achlorhydria
    risk for gastric adenocarcinomas
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9
Q

does smoking, dietary habits, or alcohol affect risk of PUD?

A

smoking yes

diet and alcohol no

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10
Q

how do PPI’s, antibiotics, and h2 receptor antagonists affect sensitivity of rapid urease test (RUT)?

A

PPIs and antibiotics decrease sensitivity bc they decrease number of h pylori. (they also decrease Urea breath test sensitivity

H2 blockers have no effect

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11
Q

which test is best for diagnosing duodenal ulcer?

which test best for confirming HP has been eradicated after antibiotics?

A

diagnose: endoscopy
eradicated: urea breath test

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12
Q

which test good for diagnosing ACTIVE H pylori infection, especially in children?

A

fecal antigen testing

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13
Q

mechanisms for increased gastrin in duodenal and gastric peptic ulcer diseases

A

duodenal: H pylori destroys D cells in antrum. less somatostatin. more gastrin -> more HCl
gastric: H pylori destroys parietal cells -> less HCl -> gastrin secretion rises

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14
Q

what drugs reduce risk of NSAID reduced gastric ulcer?

A

misoprostil (PG analogue) or lansoprazole (PPI)

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15
Q

what other thing besides gastrin is elevated in serum in patients with gastrinoma (zollinger ellison syndrome)?

A

chromogranin A. amount of elevation corresponds to the tumor volume

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16
Q

name the things that increase LES tone (lower esophageal sphincter)? (3)

things that decrease LES tone? (so many)

A

increase tone: ACh, gastrin, high protein

decrease tone: VIP and NO from vagus nerve during swalling, PGE2, fatty foods, other substances (chocolate, mint, caffeine, nicotie, ethanol), drugs (anticholinergics, Ca2+ channel blockers, beta agonists, opioids, nitrates, oral contraceptives), diabetes mellitus and scleroderma, increased intra abdominal pressure (large meals, tight clothes, obesity, pregnancy)

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17
Q

what electroneutral channel is jejunum missing? so what channel is solely responsible for electroneutral na+ reabsorption?

A

does NOT have cl/hco3 exchanger

solely relies on Na/H exchange to absorb Na+

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18
Q

what is the major electrogenic transport channel in jejunum and ileum? (for absorbing Na+)

what about for colon?

A

J and I: SGLT1 (2Na+ cotransport with glucose or galactose)

colon: ENaC (stimulated by aldosterone). SGLT is ABSENT here. note that this drives paracellular K+ secretion

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19
Q

patient comes in with watery diarrhea, hypokalemia, achlorhydria (WHDA syndrome). +/- cutaneous flushing.

what is etiology of the problem?

A

VIPoma = non beta islet cell tumor in pancreas

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20
Q

mechanism by which disease or surgical resection of ileum causes diarrhea?

A

conjugated bile acids are no longer absorbed in ileum. so when they go to colon they’re deconjugated by colonic bacteria -> incorporated into colon cell membranes -> the deconjugated bile acids activate ca2+ and camp -> increased anion secretion

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21
Q

mechanism by which short bowel syndrome and celiac dz cause secretory diarrhea?

A

reduce surface area for electrolyte absorption. ANION SECRETION IS NORMAL!!! just can’t absorb enough

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22
Q

diabetic autonomic neuropathy decreases intestinal motility so you think it wouldnt cause diarrhea, right? well wrong. it does. HOW???

note, same mechanism that happens in malabsorption of carbs and fats, pancreatic enzyme deficiency, and disruption of normal microbiota in gut

A

slowed motility causes small intestine bacterial overgrowth (SIBO) -> the bacteria deconjugate bile acids needed for lipid absorption -> metabolize the unabsorbed lipids into short chain fatty acids that stimulate crypt cell anion secretion. they also inactivate brush border enzymes needed for carb absorption -> secretory and osmotic diarrhea. explosive. not foreshadowed by cramping.

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23
Q

early dumping vs late dumping syndrome

A

early dumping: explosive diarrhea with abdominal cramping, palpitations, orthostatic hypotension, diaphoresis. 10-60 mins after eating. increased SNS -> hypoglycemia

late dumping: hypoglycemia 1-3 hours after eating. previous gastric reduction surgery. hyperinsulinemia for too long -> hypoglycemia -> sweating, hunger, tremors. NO diarrhea

24
Q

organisms that cause secretory diarrhea vs inflammatory diarrhea

A

secretory: vibrio cholerae and parahaemolyticus, ETEC, rotavirus (NSP4 toxin)
inflammatory: eneteroinvasive E. coli (EIEC) and enterohemorrhagic (EHEC), salmonella, shigella

25
Q

why is ORT effective for secretory diarrhea (v. cholerae) but not inflammatory diarrhea?

A

in secretory diarrhea, absorptive capacity of SGLT is not affected.

in inflammatory diarrhea the crypt cells replace the dying villus cells and remember crypt cells don’t absorb that much so even if you try to simulate with ORT it won’t do much

26
Q

when do you see lactoferrin in stools. where does it come from?

A

in inflammatory diarrhea, along with leukocytes. the lactoferrin is a glycoprotein expressed by activated neutrophils

27
Q

what does presence of delta gap mean in acid base disorders?

A

indicates a mixed disorder bc it means that anion gap did not increase by the equal amount that HCO3 decreased

28
Q

why do ppl with type 1 and type 2 RTA also have hypokalemia?

A

increased Hco3 in tubules (type 1 bc can’t reclaim bicarb bc can’t secrete H+ ; type 2 bc oversecrete bicarb) -> increased negative charge in lumen -> pulls k+ into lumen

29
Q

in primary metabolic alkalosis, the increase in serum hco3 is accompanied by a reciprocal decrease in serum what?

A

Cl-

30
Q

what is the biggest concern for metabolic alkalosis complications?

A

sensitizes heart to digoxin -> prolong QT interval

also hypoventilation to compensate causes hypoxemia. give them supplemental oxygen

31
Q

of the acid base disorders which one gives you Chvostek sign?

A

metabolic alkalosis. but im pretty sure then respiratory alkalosis would too bc metabolic alkalosis is milder version of resp alk…

32
Q

what things raise T4 and T3 lvls b/c they increase serum thryoglobulin? (4)

A
  1. pregnancy
  2. estrogen aka contraceptive use
  3. tamoxifen
  4. acute viral hepatitis (increases TBG release from liver)
33
Q

what things cause decreased TSH not from hyperthyroidism? (4)

A
  1. hypopituitarism (that would then cause 2ndry hypOthyroidism)
  2. acute depression or psychosis
  3. drugs. dopamine infusions and glucocorticoids
  4. elevated hCG. so like pregnancy. or germ cell tumors.
34
Q

so hypothyroidism causes reduced ejection fraction -> biventricular dilatation. can also have pericardial effusion. but know that filling pressures and PAWP are normal vs when you get dilatation from congestive cardiomyopathy

A

moving on

35
Q

do you get high protein and SAAG variable ascites in hypothyroidism?

A

why yes, yes you do

36
Q

what immune thing mediates Hashimotos?

A

CD8 cytotoxic T cells

37
Q

what things lower T4 bc they decrease TBG but it’s not hypothyroidism? (3)

A
  1. increased androgens decrease hepatic TBG production
  2. nephrotic syndrome
  3. meds. aspirin, carbamazepine, phenytoin, NSAIDs
38
Q

when can you have increase TSH and normal or hyperthyroidism? (bc normally TSH increases in response to reduced thyroid hormones/activity) (2)

A
  1. TSH secreting tumors. so primary hyper tsh lol
  2. resistance to thyroid hormone.

both of these will have high thyroid hormone levels bc of the high TSH

39
Q

neuroinhibition of what pathway causes asterixis in hepatic encephalopathy?

A

diencephalic motor centers

40
Q

what stimulates Na (in) / NH4+(out) exchange?

A

ATN II

also need to glutamine to make NH4+

41
Q

what clinical/physical finding from portopulmonary hypertension?

A

dyspnea during exertion
accentuated S2 at cardiac apex
systolic murmur (tricuspid regurg)

42
Q

what should you consider in a patient with PaO2 <70 (hypoxemia) and (A-a)O gradient is increased?

A

liver problems. hepatopulmonary syndrome.

43
Q

what is the most sensitive coagulation test for evaluating degree of hepatocellular dysfunction?

A

PT/INR

to remember, think of it as warfarin which also blocks vit K dependent clotting factors. and in liver dz the activation of those same factors is decreased

44
Q

what mixed disorder do you get from aspirin overdose?

A

AGMA + acute respiratory alkalosis

45
Q

what other 2 things are in the secretory granules with insulin? what do they do?

A
  1. amylin - decreases gastric emptying and intestinal motility and glucagon secretion. increase satiety
  2. C-peptide activates ca2+ dependent signaling pathways. deficiency may contribute to some chronic DM complications
46
Q

a2, b2, and m3 receptors have an effect on insulin. what are their effects and by what 2nd messenger system?

A

alpha 2 - decreases insulin by lowering cAMP and Ca2+

beta2 - increase insulin by raising cAMP

M3 increase insulin by raising IP3, DAG, and Ca2+

47
Q

glucagon’s effect on insulin release and mechanism.

A

increase insulin by raising plasma glucose and raising cAMP and Ca2+ inside beta cells

48
Q

how does hemochromatosis cause DM and what else do you get and what test is very sensitive for this?

A

iron deposition causes oxidative injury to beta cells
other stuff: CHF, cirrhosis, bronze skin
test: blood transferrin saturation >45%

49
Q

what is the classic triad of somatostatin secreting D cell tumor aka somatostatinoma?

A
  1. DM
  2. steatorrhea (pancreatic enzymes decreased)
  3. cholelithiasis aka gallbladder stones (decreased CKK -> decreased gallbladder contraction)
    bonus: +/- hypochlorhydria
50
Q

what clinical finding is a good marker for inherited insulin resistance?

A

acanthosis nigricans = discoloration in body folds

btw, HAIR-AN syndrome is something women get which has HyperAndrogenism, IR, and Acanthosis Nigricans. and they can develop DM if IR is bad enough

51
Q

first clinical manifestation of glucagonoma?

A

necrolytic migratory erythema = painful red rash, cyclic eruptions on face, butt, abdomen, perineum, and legs

52
Q

osmotic diuresis, like in DM, causes ____volemic ____natremia

A

hypovolemic hypernatremia

53
Q

what enzyme in what pathway converts excess glucose to sorbitol and depletes NADPH in the process?

A

aldose reductase. polyol pathway

54
Q

altered myoinositol metabolism and C-peptide deficiency is implicated in what DM complication?

A

diabetic neuropathy

so are AGEs and sorbitol but they cause everything else too lol

55
Q

biggest source of nonvolatile acid?

A

metabolism of sulfor containing and amino acids, nucleic acids, and phophoproteins.

carried by sulfuric acid, HCL, and phosphoric acid

56
Q

eating citrate can alkalanize you, bc hepatic oxidation of what produces HCO3?

A

citrate and acetate

57
Q

most important body buffer for neutralizing volatile acid (CO2)

A

Hemoglobin

Pathophysiology (3 decks)

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