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Step 1 Miscellanous > Gastrointestinal SketchyPharm > Flashcards

Gastrointestinal SketchyPharm Flashcards

1
Q

What are the afferents to the vomiting center?

A

Vomiting center = Nucleus tractus solitarius (NTS)

  1. Chemoreceptor trigger zone -
    area postrema, at base of fourth ventricular, outside BBB
    -> response to chemotherapeutic agents
  2. CN8 - vestibular system -> think of the rowing team with vests -> response to motion sickness
  3. Vagal and spinal afferents from GI tract -> response to GI irritation
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2
Q

How does the GI tract induce vomiting?

A

Think of the 1-2-3 hammer with the smiley face

Agonism of the 5HT-3 receptor via serotonin release causes nausea by stimulating vagal afferents which travel to the NTS. Serotonin release occurs when the GI tract is irritated

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3
Q

What is the first-line treatment for nausea in chemotherapy? Mechanism of action and side effects?

A

-setrons i.e. ondansetron dancer

Antagonizes 5-HT-3 receptors in the gut AND the CNS

-side effects: constipation (gut with rope around it), headache (ball hitting head), QTc prolongation (streamer around dancer), serotonin syndrome (stack of smiley faces, kinda strange since this drug is an antagonist).

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4
Q

What receptors are the primary mediators of nausea coming from each of the three major afferent pathways to the NTS/

A
  1. Area postrema - D2 receptors, NK1 receptors
  2. Vestibular system - M1 receptors (explains why vestibular nausea / motion sickness can be treated with meclizine / scopolamine / diphenhydramine)
  3. GI tract - 5HT3 receptors
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5
Q

What psych drugs are good at stopping nausea and how do they work? Adverse effects?

A

Metoclopramide, prochlorperazine

D2 receptor antagonism at area postrema (chemoreceptor trigger zone)

Adverse effects: Drowsiness (guy sleeping), dystonia / Parkinsonism (EPS, guy wearing hat), tardive dyskinesia (Sticking tongue out), NMS (chicken rigidity), elevated prolactin levels (milk coming out of his nose), QT prolongation (QT streamer on the judge’s table)

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6
Q

What two medications are used for gastroparesis and which is used most commonly? What are there mechanisms of action?

A
  1. Metoclopramide - used most commonly - D2 receptor antagonist, and 5HT4 agonist - me tickle guy hanging from the D2 ropes
  2. Domperidone - D2 receptor antagonist

The D2 receptor inhibits Ach release and thus motility if not blocked. (Makes sense because dopamine is basically a sympathetic hormone which should stop bowl motility)

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7
Q

What is the expensive but highly effective drug used as a last line for vomiting during chemotherapy?

A

Aprepitant - think participant in sketchy

(pla)NK1 / Substance P(ee) receptor antagonist in area postrema

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8
Q

How does gastrin increase acid secretion by the parietal cells?

A

Activates CCK-B receptors in two places.

Major effect:
1. Enterochromaffin-like cells -> stink of the gastrin blower stimulating the bee-hive. Increases histamine release from ECL cells which stimulates H2 receptors to increase cAMP.

Minor effect:
2. Parietal cells - directly increases Gq signalling (along with M3 receptors) to increase stimulation of H+/K+ ATPase. Think of the gas tank connected to the lemonade maker.

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9
Q

What are the primary stimulators of gastrin release?

A
  1. Gastrin-releasing peptide - released from the vagus nerve onto G cells. This is an additional effect on top of the M3 stimulation of parietal cells from the vagus nerve.
  2. Alkalinization of stomach
  3. Stomach distension / sensation of amino acids / peptides in the stomach.
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10
Q

What is the final vagal effect on digestion other than stimulation of the G cells (via GRP) and stimulation parietal cells?

A

Inhibitory to somatostatin cells, so everything can be upregulated.

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11
Q

What is the H2 receptor blocker with the most side effects and what are they?

A

Cimetidine - think cimetidine side walk side effects

Potent inhibitor of CYP450, so rarely used (think of the truck)

Antiandrogen - Can cause gynecomastia and hyperprolactinemia - think of boobs in sketchy and milk shooting from nose

Also decreases renal excretion of creatinine (along with trimethoprim) - remember from renal

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12
Q

What are the adverse drug reactions by all H2 receptor antagonists?

A

Headache, drowsiness, fatigue, can cross BBB and cause confusion and dizziness

-> relatively worse with cimetidine

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13
Q

What are the potential adverse effects of PPI’s?

A

Increased risk of C. difficile infection - acid needed to prevent, think of chocolate fountain in sketchy

Increased risk of pneumonia - think of girl with exposed lungs coughing - due to acid needed to clear bacteria

Hypomagnesemia with prolonged use - think of magnets.

Decreased divalent cations absorption in general - Can also be associated with hypocalcemia and low iron (H+ needed to absorb these)
-> an important cause of OSTEPOROSIS (think of the broken wagon axle)

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14
Q

What are three osmotic laxatives which can be used to improve constipation / bowel prep for surgery?

A
  1. Polyethylene glycol - think of the PEG in the drain
  2. Mg+2 - Makes you go, milk of magnesia
  3. Lactulose - also used in combination with rifaximin (fisherman) for treatment of hepatic encephalopathy. Remember dis.
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15
Q

What are bulk-forming laxatives and give a few examples?

A

Drugs which increase fecal mass, resulting in stimulation of peristalsis

  • > Psyllium - seaweed
  • > methylcellulose
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16
Q

What is the mechanism of action of docusate as a laxative?

A

Think of the water penetrating the canoe at the DOCK

-> surfactant agent which facilitates the penetration of stool by water and lipids

17
Q

What are the two stimulant laxatives and what is their relative strength?

A

Senna - slow-acting, weak - think of the senna suntan lotion stimulating that man’s belly in sketchy

Bisacodyl - very strong

These both stimulate the enteric nervous system directly and produce strong but brief peristaltic movements

18
Q

What is the main side effect of Senna?

A

Think of senna suntan

-> melanosis coli - pigmentation of the GI tract

19
Q

What are two opiate drugs used in the treatment of non-infectious diarrhea? Which one causes BBB and what is it given with?

A
  1. Loperamide - lop-eared bunnies, stimulate GI peristalsis back and forth so there is no net movement
    - > can cross BBB
  2. Diphenyoxylate - dolphins, given in combination with atropine to slow bowel movements and also to reduce dependence as diphenoxylate also binds mu receptors in the brain (able to cross BBB somewhat)
20
Q

What is a VIPoma?

A

“Pancreatic cholera” - it is a pancreatic islet cell tumor which secretes VIP

Causes WDHA syndrome

Watery diarrhea - via stimulation of Na/Cl/HCO3- from intestines
Hypokalemia
Achlorhydria - inhibits gastric acid secretion

21
Q

How is VIPoma treated?

A

Think of the VIP crab on the wall

Treated same as carcinoid tumor -> via Ocretotide (stop sign)

22
Q

What prostanoid is essential the opposite of TXA2?

A

Prostacyclin (PGI2) - produced by COX2, inhibits platelet aggregation and promotes vasodilation -> inflammation increases the bloodflow to an area and prevents blockage (Same reason why your mast cells release heparin)

TXA2 - produced by COX1, promotes platelet aggregation and vasconstriction (The target of aspirin)

23
Q

Which Cox is responsible for producing prostaglandins which protect the gastric mucosa?

A

COX-1

  • > think of the catcher with the GI gear standing next to the COX-1 head coach at the batter’s box
  • > reason why celecoxib (COX-2 selective) has less GI side effects
24
Q

What is the overall function of COX-2?

A

Mediates inflammation

  • > increased vascular permeability, fever, and pain
  • > COX-2 is the primary thing that we want to block for pain-killing and anti-acute inflammatory effects
25
Q

What are considered the high risk vs low risk NSAIDs for causing ulcers?

A

High risk - indomethacin, ketoroLAC (mainly used as analgesic per sketchy), aspirin, piroxicam (think of the sox cam in sketchy)

Low risk: Ibuprofen, diclofenac, naproxen, meloxicam (more COX-2 per sketchy, thus less side effects), especially celecoxib

26
Q

What lab coagulation test can NSAIDs effect?

A

By blocking TXA2 effects via COX-1 inhibition, they can prolong the bleeding time.

-> NSAIDs should be avoided in patients with platelet defects

27
Q

What is one extra side effect of concern with indomethacin?

A

Think of the floating bone balloon next to the lithium liftium
-> can cause aplastic anemia

28
Q

What type of RTA can NSAIDs cause and how?

A

Type 4 renal tubular acidosis (hyperkalemic hypoaldosteronism)

  1. PGE2 is the signal by macula densa cells for renin secretion by juxtaglomerular cells (modified smooth muscles of afferent arteriole)
  2. Loss of PGE2 also prevents dilation of afferent arteriole -> loss of GFR = hyperkalemia
29
Q

What is the treatment for aspirin overdose?

A

Think of the guy under the bases loaded sign with the eye paint on

  1. Charcoal - activated charcoal within two hours will scavenge whatever remains from the stomach
  2. IV bicarbonate - to treatment metabolic acidosis and alkalinize the urine (Traps aspirin, a weak acid, in urine to facilitate excretion)
30
Q

What are two important contraindications of NSAIDs?

A
  1. Third trimester of pregnancy - due to closure of PDA

2. Chronic kidney disease - due to reduction in GFR. Minimize use in those at risk for AKI.

31
Q

What class of drug is celecoxib? Who should it be avoided in?

A

Think of the rotten eggs being thrown on the guy who is celebrating (it is a SULFA drug!, therefore can inherently cause AIN)

Avoid in patients with angina / post MI -> increased thrombosis risk (selective COX-2 without COX-1 inhibition).

32
Q

Would acetaminophen be better for osteoarthritis or rheumatoid arthritis? How does the antidote work?

A

Osteoarthritis - since it is only a good analgesic / antipyretic, but has no antiinflammatory effect (not good for RA when anti-inflammation is needed)

Antidote - regenerates callular glutathione -> hepatocytes can further inactivate NAPQI

33
Q

How does elevated triglycerides cause pancreatitis?

A 
Fatty acids overwhelm the binding capacity of serum albumin -> direct toxicity to pancreatic cells
#440

Step 1 Miscellanous (40 decks)

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