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GIT Flashcards

KCP 2

1
Q

pathology

What is Hirschsprung disease?

A

dilatation of colon proximal to inactive segment

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2
Q

pathology

What causes Hirschsprung disease?

A

caused by absence of enteric ganglia (parasympathetic postganglionic neuron cell bodies) in lower part of colon.

Congenital: failure of migration of neural crest to form myenteric plexus

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3
Q

embryology

How is primitive gut tube formed?

A

Incorporation of yolk sac into embryonic disc during craniocaudal and lateral folding of embryo

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3
Q

embryology

Which germ layer give rise to different tissues of GIT?

A

Endoderm: endothelial + glands of GIT
splanchnopleuric mesoderm: muscular, connective tissue

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4
Q

embryology

What is vitelline duct?

A

Connects primitive gut tube with yolk sac

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5
Q

embryology

Embryological basis of errors in esophageal development

A
  1. Esophageal stenosis: incomplete esophageal recanalisation
  2. Achalasia cardia/achalasia: failure of relaxation of musculature in lower part of esophagus/ failure of the lower esophageal sphincter (LES) to relax that is caused by the degeneration of inhibitory neurons within the esophageal wall
  3. Tracheosophageal fistula: incomplete fusion of tracheoesophageal septum
  4. Short esophagus: failed to elongate, stomach exists inside thoracic cavity, cause congenital hiatal hernia
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6
Q

embryology

Developmental process of stomach

A

Along longitudinal axis: 90 clockwise
Along ant.-post. axis: pyloric part right and upwards, cephalic part left and downwards

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7
Q

embryology

Developmental process of stomach with errors

A

Congenital hypertrophic pyloric stenosis: hypertrophic of circular muscle at pylorus

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8
Q

embryology

Source and developmental errors of pancreas

A

Source: endoderm of developing duodenum
Error: annular pancreas- ventral pancreas splits and forms a ring around duodenum, duodenum stenosis

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9
Q

embryology

Derivatives of ventral and dorsal pancreatic bud

A

Ventral bud: uncinate process and head of pancreas
Dorsal bud: remaining parts of pancreas

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10
Q

embryology

Derivatives of developing mesentery

A

Dorsal mesentery:
-dorsal mesogastrium/greater omentum
-dorsal mesoduodenum
-mesentery proper
-dorsal mesocolon
Ventral mesentery
-falciform ligament
-lesser omentum

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11
Q

embryology

Which artery form the axis of primary intestinal loop?

A

SMA

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12
Q

embryology

Rotation of midgut

A

-physiological herniation (6th week): 90 counterclockwise (entering yolk sac)
-retraction (10th week): 90 counterclockwise (cecal bud goes upwards at cranial limb)
-total retraction: 90 counterclockwise (cecum starts descending after 270)

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13
Q

embryology

Developmental error of midgut

A
  1. Rotation issue
    -non rotation
    -reverse rotation: all rotations clockwise
    -subhepatic cecum and appendix
  2. Recanalization failure
    -exomphalos/omphalocele: failure of physiological herniation
    -congenital umbilical hernia: ant. abdominal wall defect
  3. Vitelline duct issue
    -vitelline cyst
    -vitelline/umbilical fistula
    -Meckel’s diverticulum
    4.duodenum
    -atresia and stenosis
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14
Q

embryology

Developmental errors of hindgut

A
  1. Rectal fistulae: imperforated anus and rectal atresia
  2. Imperforate anus: got anal pit and cloacal membrane
  3. Congenital megacolon/ Hirschsprung’s disease:parasympathetic fails to develop/ enteric NS
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15
Q

pharm PUD

What are the drugs used for peptic ulcer disease?

A
  1. Agents that reduce intragstric secretion/acidity
    - proton pump inhibitors (PIP): omeprazole
    - H2-receptor antagonists:cimetidine, ranitidine
    - anti-muscarinic agents: pirenzepine
    - antacids: aluminium hyroxide, calcium carbonate, Mg(OH)2, NaHCO3
  2. Mucoprotective agents
    -prostaglandin analogues: misoprostol
    -miscellaneous: bismuth compounds, sucralfate
  3. Drugs for treatment of H. pylori infection
    -triple therapy (PPI+clarithromycin+amoxicillin/metronidazole)
    mnemonic:OCLAM
    -quadruple therapy (PPI+metronidazole+bismuth subcitrate+tetracycline)
    mnemonic: OBMT
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16
Q

pharm PUD

therapeutic use of PPI (omeprazole)

A

zollinger ellison syndrome (produce too much gastric acid)

dose reduction required in severe liver failure

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17
Q

pharm PUD

MOA of omeprazole

A

irreversible inhibition of proton pump H+/K+ ATPase> inhibit basal and stimulated acid secretion

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18
Q

pharm PUD

MOA of H2 receptor blockers (cimetidine, ranitidine)

A

competitively and reversibly block H2 receptor on parietal cells>adenylyl cyclase not activated>protein kinase not activated>inhibits histamine induced gastric secretions

promote mucosal healing and decrease pain

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19
Q

pharm PUD

AE of H2 antagonist: cimetidine and ranitidine

A

gynecomastia
impotence
galactorrhea
can cross BBB

decrease metabolism of CP450 inhibitor

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20
Q

pharm PUD

MOA of anticholinergic drug (pirenzepine)

A

block muscarinic M1 receptors on parietal cells> no Ca2+>protein kinase not activated> PP not activated>inhibit gastic acid secretion

used together w/ H2 receptor blockers like cimetidine, ranitidine

decrease pain in PU

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21
Q

pharm PUD

MOA of antacids (sodium bicarb, calcium carbonate, aluminium OH, magnesium OH)

A

binds to HCL, increase pH, neutralise gastric acid, inhibit pepsin

sodium bicarb causes stomach distension due to liberation of CO2

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22
Q

pharm PUD

AE of aluminium OH and magnesium OH

A

aluminium OH: constipation
magnesium OH: diarrhea

*no stomach distension

*when combine can avoid both AE

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23
Q

pharm PUD

MOA of sucrose octaphosphate+Al2(OH)3 (sucralfate)

A

in acidic condition, it dissociated into sucrose octaphosphate and an antacid

SO + positively charged protein (that coats ulcer)>inhibits pepsin>promotes healing

do not administer w/ H2 blockers

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24
Q

pharm PUD

therapeutic uses of sucralfate

A

benign gastric and duodenal ulcers, chronic gastritis

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25
Q

pharm PUD

MOA of prostaglandin analogue (misoprostol)

A

decrease HCL secretion
increase mucus & bicarb secretion
increase BF to mucosa to promote healing

therapeutic effect: prevent NSAIDs induced PU

CI in pregnancy

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26
Q

pharm PUD

MOA of colloidal bismuth (bismuth)

A

forms precipitate w/ mucus>cover ulcer with protective coat>promote healing

decrease pepsin and increase mucus, HCO-3 secretion

has bactericidal effect

AE: black stool, teeth discolouration

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27
Q

pharm PUD

MOA of drugs used for H. pylori

A
  1. triple therapy [OCLAM]
    O:omeprazole
    CL: clarithromycin
    AM: amoxicillin/metronidazole

-PPI (omeprazole): increase stomach pH, antimicrobial
-antibacterial (clarithtromycin, amoxicillin/metronidazole)
2.quadruple therapy [OBMT]
-PPI:omeprazole
-antibacterial: tetracycline,amoxicillin/metronidazole
-bismuth

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28
Q

anatomy

Which muscle forms the inguinal ligament?

A

External oblique

free inferior border of aponeurosis=inguinal ligament

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29
Q

anatomy

A 45yo man presents with an infected ulcer midway between epigastric and umbilical regions. Which lymph node is most likely to be enlarged?

A

Axillary.
lymphatics from region above the level of umbilicus drain to AXILLARY LN. Those beow level of umbilicus drain to SUPERFICIAL INGUINAL LN. Umbilicus is known as the water-shed line.

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29
Q

anatomy

A patient comes back to the surgeon’s clinic one month after an operation for obstructed left inguinal hernia has been done. He complains of numbness and sensation of pins and needles over the skin of medial side of left thigh and anterior part of left half of the scrotum. Which nerve is most likely damaged during op?

A

ilioinguinal

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30
Q

anatomy

posterior layer of rectus sheath ends at

A

arcuate line
Midway between umbilicus and symphysis pubis, aponeurosis of all three muscles forming rectus sheath reflect anterior to rectus abdominis muscle. Internal oblique and transversus abdominis which form posterior layer of rectus sheath ends at this point producing a semilunar line called arcuate line.

arcuate line=Douglas’ line=linea semicircularis

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30
Q

anatomy

A med student palpates the margin of superficial inguinal ring of a healthy male patient. Which bony landmark is used to identify the superficial ring?

A

pubic tubercle
Superficial inguinal ring is opening in aponeurosis of external oblique muscle. After the ring the aponeurosis continues as outermost covering of spermatic cord. Although the ring lies over pubic crest (it is not palpable), the ring is superior and lateral to pubic tubercle.

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31
Q

anatomy

muscle of soft palate (palatopharyngeus,
Palatoglossus) are innervated by

A

trigeminal and vagus nerve.

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32
Q

anatomy

appendicectomy: which quadrant of the abdomen will be located to give incision?

A

right iliac fossa.
terminal part of ileum, appendix and cecum are located at R iliac fossa. McBurney point is max tender in acute appendicitis.

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33
Q

anatomy

While operating for indirect inguinal hernia, a surgeon observes an unusal rapid oozing of blood. The bleeding needs to be controlled. Which artery is most likely injured?

A

inferior epigastric.
it lies immediately medial to deep inguinal ring. As the neck of hernia sac is indirect hernia descend through deep inguinal ring.

34
Q

anatomy

Conjoint tendon is formed by?

A

common aponeurosis of internal oblique and transverse abdominis muscle

35
Q

histology

special features of esophagus

A

stratified (many layers of pancakes) squamous (dark border at the bottom)

36
Q

histology

special features of stomach

A

-ridges on top (knuckles, cheerios/lil circles)
-when you see a flat line, that’s muscularis mucosa, above this is mucosa.
-gastric pit (top opening) and glands (bottom)
-has serosa

37
Q

histology

special features of small intestine

A

-ridges on top (fingers)=villli
-simple columnar w/ goblet cells
-inside villli is lamina propria
-intestinal crypts are the base of villi
-see the bottom edge of mucosal layer>muscularis mucosa
-duodenum (retroperitoneal)>adventitia
-jejenum and ileum have serosa
-duodenum (brunners glands=cheerios), ileum (peyer’s patches)

38
Q

histology

special features of large intestine

A

-ridges on top (smaller than stomach, mucosa layer is smaller, looks regular and organised than stomach)
-see the bottom edge of mucosal layer>muscularis mucosa
-ascending descending colon>adventitia, sigmoid, rectum, transverse>serosa
-no villi
-goblet cells (white bubbly cells) more numerous

39
Q

histology

all organs of digestive tract have 4 layers

A
  1. mucosa:
    -epithelium: stratified squamous (mouth-esophagus, anal canal), simple columnar (stomach to rectum
    -lamina propria (anchoring epithelium):
    -muscularis mucosa
  2. submucosa:
  3. muscularis externa
    -outer longitudinal
    -inner circular
    -innermost oblique (only in stomach)
  4. adventitia/serosa
    -organs within the peritoneum have serosa
    -organs which are retroperitoneal/not within the abdominal cavity have adventitia

refer to YT: digeestive system histology by anatomy hero

40
Q

pharm IBD

Drugs used for treatment of inflammatory bowel disease: Crohn’s disease and ulcerative colitis

A
  1. anti-inflammatory drugs
    a) sulfasalazine (5-aminosalicylic acid+sulfapyridine)
    b) glucocorticoids: prednisolone, budesonide
  2. immunomodulatory agents
    a) thiopurine derivatives: azathioprine, 6-mercaptopurine
    b) methotrexate
    c) cyclosporine
  3. biological agent
    a) infliximab
    b) antibiotics: metronidazole, ciprofloxacin, amoxicillin-clavulanate, piperacillin-tazobactam
41
Q

pharm IBD

MOA of anti-inflammatory drugs: sulfasalazine

A

sulfasalazine (5-aminosalicylic acid + sulfapyridine)

5-ASA and SPD are bonded tightly together by an azo bond. This is broken when it reaches the colon by colonic bacteria.

azo bond broken> 5-ASA remains in colon & has anti-inflammatory effect> SPD enters bloodstream & has immunomodulatory effects.

Hence, 5-ASA provides relief of acute symptoms. SPD is used in rheumatoid arthritis.

42
Q

pharm IBD

AE of sulfasalazine

A

sulfa drugs are commonly associated with allergic reactions & nephrotoxicity

42
Q

pharm IBD

therapeutic use of sulfasalazine

A

-mild to moderate UC
-use with glucocorticoids for severe UC

42
Q

pharm IBD

AE of sulfasalazine

A

sulfa drugs are commonly associated with allergic reactions & nephrotoxicity.

43
Q

pharm IBD

MOA of anti-inflammatory drugs: glucocorticoids (prednisolone, budesonide)

A

GC + transcortin>complex released into cytoplasm>binds to GC receptor and activate it> HSP-70 & IP (proteins) are removed> activated complex receptor now goes to nucleus to act on GC responsive element (GRE)> transcription occurs> synthesis of mRNA which moves into cytoplasm and synthesise protein> protein inhibits phospholipase A2

-inhibits phospholipase A2>decrease in free arachidonic acid>reduced prostaglandin, thromboxane and leukotriene

transcortins transport steroid hormones (esp. cortisol) in blood.

44
Q

pharm IBD

AE of glucocorticoids

A

Cushing syndrome: buffalo hump, moon face, thinninf of skin, increased abdominal fat, muscle wasting, easy bruising, poor wound healing, cataract

45
Q

pharm IBD

therapeutic effects of glucocorticoids

A

-moderate to severe IBD
-prednisolone use in Crohn’s
-budesonide use in ileocecal crohn’s
-glucocorticoids enema use in disease limited to rectum and left colon

46
Q

pharm IBD

MOA of immunosuppressive/immunomodulatory agents: thiopurine derivatives (azathioprine, 6-mercaptopurine)

A

-inhibit purine biosynthesis
-inhibit cell proliferation

patient with low TPMT (enzyme) should be given lesser dose of 6-MP, high TPMT should give higher dose

47
Q

pharm IBD

drug-drug interaction of thiopurine derivatives (azathioprine, 6-mercaptopurine)

A

6-MP interacts with allopurinol (treats gout and hyperuricemia). Taken together will reduce XO, increasing concentration of 6-MP, leading to bone marrow suppression

48
Q

pharm IBD

MOA of immunomodulatory agent: methotrexate

A

irreversibly bind to DHFR and prevent conversion of folic acid to DHF and THF

-inhibit purine and pyrimidine synthesis
-inhibit DNA synthesis

Folic acid>DHF>THF>purine, pyrimidine>DNA

AE:cause megaloblastic anemia

49
Q

pharm IBD

therapeutic effect of methotrexate

A

only used in IBD pt if they are steroid resistant or steroid dependent

AE: megaloblastic anemia

50
Q

pharm IBD

MOA of immunomodulatory agent: cyclosporine

A

anticancer drug
-inhibit calcineurin

often used after organ transplant

only used when other therapy failed

calcineurin activates T cell activity

51
Q

pharm IBD

MOA of biological agent: antibiotics

A

metronidazole, ciprofloxacin, amoxicillin-clavulanate, piperacillin-tazobactam
-clavulanate is a beta lactamase inhibitor (help overcome bac resistance to penicillin)

treat severe IBD, perforating/fistulizing complications of crohn’s

52
Q

pharm IBD

MOA of biological agent: infliximab

A

anti-TNF alpha monoclonal antibody
-neutralise TNF-alpha
-AE:TB

tnf-alpha: a cytokine that mediates Th1 immune response (crohn’s)

high cost hence last choice

53
Q

pharm IBD

descriptions of the below drugs:
infliximab
sulfasalazine
methotrexate
mercaptopurine
glucocorticoids
cyclosporine

A

infliximab: monoclonal antibody
sulfasalazine: a drug that has 2 components
methotrexate: cause megaloblastic anemia
mercaptopurine: should not be given with allopurinol
glucocorticoids: inhibit phospholipase A2
cyclosporine: calcineurin inhibitor

54
Q

pharm motility disorders

antiemetic drugs

A
  1. 5-HT3 antagonists: ondansetron
  2. antidopaminergics: domperidone, metoclopramide
  3. neurokinin receptor antagonist: aprepitant
  4. anticholinergic: scopolamine
  5. antihistaminic: cyclizine, meclizine, doxylamine
55
Q

pharm motility disorders

drugs for constipation

A
  1. bulk forming laxative: bran, psyllium, ispaghula
  2. stool softeners: docusates, liquid paraffin
  3. osmotic laxatives: Mg salt, Na salt, lactulose
  4. stimulant laxatives: bisacodyl, senna, castor oil
56
Q

pharm motility disorders

drugs for diarrhoea

A
  1. opioids: diphenoxylate, loperamide
  2. antispasmodics: dicyclomine
  3. zinc
  4. ORS
  5. antibiotics: tetracycline, cotrimoxazole, norfloxacin, ciprofloxacin, metronidazole
57
Q

pharm motility disorders

MOA of 5-HT3 antagonist: ondansetron

A

inhibits vomiting center and chemoreceptor trigger zone (CRTZ)
blocks peripheral 5-HT3 receptors on extrinsic intestinal vagal & spinal afferent nerve
used in chemotherapy induced emesis (CIE)-first line] and post op.

add on corticosteroid (dexamethasone) to increase efficacy

corticosteroids alone do not work as antiemetics

58
Q

pharm motility disorders

MOA of antidopaminergics: domperidone, metoclopramide

A

block D2 receptors in CRTZ, loss of inhibition myenteric motor neuron, increase ACh, increase intestinal motility

increase esophageal peristaltic amplitude
increase LES pressure
enhance gastric emptying

used in motion sickness, postop vomiting

metoclopramide> extrapyrimidal symptom coz cross BBB,domperidone can’t

59
Q

pharm motility disorders

MOA of neurokinin receptor antagonist: aprepitant

A

blocks neurokinin receptors in CRTZ of area postrema

used with 5HT3 antagonist and corticosteroids in CIE

60
Q

pharm motility disorders

MOA of anticholinergic: scopolamine

A

non-selective competitive inhibitor of M1-M5 muscarinic ACh receptors

used in motion sickness

AE: cycloplegia (loss of accomodation due to ciliary muscle paralysis)

61
Q

pharm motility disorders

MOA of antihistaminic: cyclizine, meclizine, doxylamine

A

used in morning sickness in pregnancy

62
Q

pharm motility disorders

MOA of bulk forming laxatives: bran, psyllium, ispaghula

A

soluble fibers, increase water absorption in intestinal lumen, increase fecal mass, bowel is stretched, stimulate peristalsis

used in simple constipation

take w/ adequate water to prevent dehydration

63
Q

pharm motility disorders

MOA of stool softeners: docusates, liquid paraffin

A

anionic surfactant, lowers surface tension of the stools

emulsifies colonic contents, increase penetration of water into feces

AE: hepatotoxicity on prolonged use

64
Q

pharm motility disorders

MOA of osmotic laxatives: Mg salts, Na salts, lactulose

A

Mg salts: act on SI & LI, retain water, increase mass, increase peristalsis

release cholecystokinin, increase intestinal secretions, promote peristalsis

Na salts: act on SI & LI, increase osmotic pressure, draws water into lumen, increase peristalsis

Mg and Na used in food/drug poisoning, after purge in tapeworm infestations, bowel prep before surg

lactulose (colonic acidifier coz it decreases NH4 in blood): acidic when broken down, more osmotically active compounds, water retention

use to treat hepatic encephalopathy *pH stool is low>ammonia produced in colon coverted to ionised NH4+>decreased ammonia absorption

65
Q

pharm motility disorders

MOA of opioids for anti-diarrhea: diphenoxylate (less potent, can cross BBB), loperamide (more potent, can’t cross BBB)

A

activate parasympathetic opioid receptors in ENS, inhibit ACh release, decrease peristalsis

enhance absoprtion

*should not be used in infective diarrhoea & kids
*at usual dose it lacks analgesic effects

65
Q

pharm motility disorders

MOA of stimulant laxatives: bisacodyl, senna, castor oil

A

accumulate water & electrolyte, increase motility by acting on myenteric plexus.

irritate intestinal mucosa, stimulate motor activity

66
Q

pharm motility disorders

MOA of antispasmodics: dicyclomine

A

relaxation of smooth muscle of GIT
reduce GIT spasm
relieve abdominal pain

67
Q

pharm motility disorders

MOA of drugs in diarrhea:
zinc
ORS
antibiotics

A

zinc: reduce fluid secretion in intestines, strengthen immune response, regenerate intestinal epithelium

ORS: salt containing Na, K , Cl, trisodium citrate and glucose constituted water. ORS don’t stop diarrhea but maintains electrolyte balance

antibiotics: tetracycline, cotrimoxazole, norfloxacin, ciprofloxacin, metronidazole. NOT USED in IBS, celiac disease, rotavirus infextion etc

68
Q

pharm ART

Drugs for retroviral infections (HIV-1, HIV-2)

A

Maraviroc (CCR5 antagonist)
Enfuvirtide (Fusion inhibitor)
Zidovudine, abacavir, lamivudine (NRTI)
Tenofovir (NtRTI)
Nevirapine, efavirenz, delavirdine (NNRTI)
Raltegravir (integrase strand transfer inhibitor)
Ritonavir (protease inhibitor)

69
Q

pharm ART

Adverse effect of NRTI: zidovudine

A

anemia

‘get zid (rid) of hb’

70
Q

pharm ART

Drugs in nucleoside reverse transcriptase inhibitor (NRTI/NtRTI)

A

zidovudine
lamivudine
tenofovir (NtRTI)
abacavir

71
Q

pharm ART

AE of NRTI

A

peripheral neuropathy
bone marrow suppression (treat with granulocyte colony stimulating factor)
lactic acidosis
pancreatitis
anemia (specific to zidovudine)

72
Q

pharm ART

Drugs in non-nucleoside reverse transcriptase inhibitors (NNRTI)

A

Delavirdine
Efavirenz
Nevirapine

‘NO NO, not in the DEN’

73
Q

pharm ART

AE of NNRTI

A

hepatotoxicity & skin rash, vivid dreams (specific to efavirenz), efavirenz +delavirdine CI in pregnancy

74
Q

pharm ART

AE of efavirenz

A

vivid dreams

‘efa-VIVIDz’

75
Q

pharm ART

Drugs in protease inhibitors
(-navir)

A

ritonavir
lopinavir
atazanavir

76
Q

pharm ART

AE of protease inhibitor

A

hyperglycemia
GI effects
lipodystrophy
nephropathy
P450 inhibitor (specific to ritonavir)

‘-PRO’

‘liPROdystrophy
hyPROglycemia
PROfuse diarrhea’

protease inhibitors NAVIR allow for mature viruses

77
Q

pharm ART

AE of ritonavir

A

P450 inhibitor

‘ritONavir turns ON other drugs by inhibiting P450’

78
Q

pharm ART

Drugs in integrase strand transfer inhibitors INSTI (-tegaravir)

A

raltegravir
dolutegravir
elvitegravir

79
Q

pharm ART

AE of INSTI

A

increase creatine kinase

‘InteCKrase’

80
Q

pharm ART

Drug that targets GP41 on HIV virus

A

enfuvirtide

prevent penetration/fusion inhibitor

81
Q

pharm ART

Drug that inhibits CCR5 receptor on host cells

A

maraviroc

prevent attachment

think of ‘MAZDA CX5’

82
Q

pharm ART

HAART: highly active antiretroviral therapy includes:

A

2 NRTI + INSTI/boosted PI/NNRTI

*need to check gender and pretreament CD4 cell count if considering Nevirapine (NNRTI)
*need to test HLA B 5701 if considering Abacavir (NRTI)

83
Q

path

viral hepatitis
-pathophysiology

A

-inflammation of the lobules and portal tracts, cytotoxic/CD8+ T-cell mediated hepatocyte apoptosis
-periportal zone of liver is first affected (zone 1)
-increase ALT more than AST

*hep A: Councilman bodies/eosinophilic globule of apoptotic hepatocytes
*hep B: ground glass/eosinophilic appearance due to accumulation of HBsAg in infected hepatocytes
*hep C: IV drug use
*hep D: always need hep b to replicate
*hep E: high mortality in pregnant women

AG1 (2 decks)

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