Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medical Physiology > GI Disorders > Flashcards

GI Disorders Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

what gastroduodenal disorders is H pylori indicated in?

A
  1. acute and chronic gastritis 2. gastric and duodenal ulceration 3. gastric cancer 4. gastric MALT lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where is h pylori found

A

present in gastric antrum and lives beneath mucus layer, can secrete urease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how does urease help H pylori?

A

environmental modulator, protects microorganism from toxic effects of the gastric acidity by raising the pH of its microenvironment OR maintains intracellular nitrogen balance in H pylori (excess nitrogen inside cells produced by fast catabolism of AA could be disposed of by excretion via urea cycle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does urease do

A

hydrolyses urea to carbonic acid/bicarbonate and ammonia/ammonium; contributes to buffering the acidic pH around the bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does the presence of arginase suggest?

A

that H pylori has a complete urea cycle which acts as an effective mechanism to extrude excess nitrogen from cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the urea cycle that h pylori does

A

arginase converts water and arginine to urea, which is then broken down by urease to ammonium and CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are 2 roles fore urease?

A
  1. hydrolysis of urea by urease outside of cells avoids the formation of a concentration gradient that may drive urea/metabolic product back into the cytosol
  2. compatible with an acid-protection function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

sources of urea?

A
  1. H pylori produces its own urea from arginine as part of its own urea cycle
  2. host urea formed in the liver from protein deamination. carried to kidneys for renal use and excretion. urea carried by circulatory system from liver to kidneys
  3. urea is present in saliva and gastric secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is BUN

A

blood urea nitrogen – measures amount of urea nitrogen found in blood. normal is 6-20mg/dL of BUN, high BUN indicates kidney problem bc kidneys are not able to remove urea from the blood normally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the purpose of a highly acidic gastric environment

A

kill microorganisms and activate pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how can h pylori survive in a ph 1-3 environment?

A
  1. lives in the alkaline mucous produced by gastric mucosa
  2. generates ammonium ion through urease on urea from itself and the host
  3. helical body shape not used to corkscrew, but H modifies its microenvironment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe how h pylori modifies its microenvironment

A

mucin is the main protein in mucus.

mucin is in gel form at acidic pH near the gastric lumen.

at neutral pH, mucin is a viscous liquid, allows h pylori to swim near cell surface.

H pylori then binds to different mucins on cell surface.

ammonium ion production via ureas damages the plasma membrane facilitating cell penetration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does mucin look like at acidic ph

A

gel like at gastric lumen to form barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does gastrin look like at neutral ph

A

viscous liquid, so allows h pylori to swim near cell surface. damages cells via ammonium ion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what causes zollinger ellison syndrome?

A

gastrin producing tumors release abnormal amounts of gastrin, leading to excess gastric acid in the stomach and duodenum. this causes multiple peptic ulcers to form in the lining of the duodenum.

1 or more tumors in pancreas, duodenum or both.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

who is most commonly affected by zollinger ellison syndrome?

A

30-50yo males and those with the MEN-1 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

possible indicators of ZES

A

peptic ulcers in the absence of H pylori infections or NSAID use

OR

severe peptic ulcers that bleed or cause perforations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ZES symptoms

A

burning abdominal pain

n/v/d

weight loss

severe gastroesophageal reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how to treat ZES

A

H2 receptor antagonists

PPI

surgical resection or removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is peptic ulcer disease

A

ulcer (greater than 0.5cm) of an area of the GI tract that is usually acidic and painful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how are ulcers made worse?

A

caused or worsened by drugs like aspirin or other NSAIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

where do most ulcers arise?

A

more in the duodenum than the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are 3 common causes of ulcers?

A
  1. stress
  2. diet
  3. h pylori
  4. (4% caused by malignant tumor like ZES)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

difference between IBS and IBD

A

IBS is a cluster of symptoms without a tangible cause.

IBD is a heterogenous group of disorders with a tangible cause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is IBS

A

irritable bowel syndrome, functional bowel disorder with a characteristic cluster of symptoms in the ABSENCE OF DETECTABLE STRUCTURAL ABNORMALITIES

26
Q

what causes IBS

A

unknown, intangible cause.

27
Q

common theory of IBS cause

A

disorder of the interaction between the brain and the GI tract

(interstitial cells of cajal? myenteric plexus?)

may be abnormalities in gut glora or immune system

28
Q

what is IBD

A

heterogeneous group of disorders characterized by various forms of chronic mucosal and/or transmural inflammation of the intestine (all or part of digestive tract)

29
Q

what does IBD include?

A

ulcerative colitis and crohn’s disease

30
Q

what characterizes IBS

A

spastic colon

chronic abdominal pain

discomfort

bloating

alteration of bowel habits in the absence of any detectable organic cause

31
Q

how can IBS be classified further?

A

IBS-D (diarrhea predominant)

IBS-C (constipation predominant)

IBS-A (alternating stool pattern, pain predominant)

32
Q

relationship with IBD and CRC

A

IBD people with crohn’s disease or ulcerative colitis are at higher risk for developing CRC than the general population

33
Q

incidence of cRC

A

147000 new CRC are diagnosed

57000 die

second leading cause of cancer related deaths in the country

34
Q

what causes crohn’s disease

A

inherited genes

autoimmune repsonses

environmental factors

35
Q

symptoms of crohn’s disease

A

persistent diarrhea

abdominal cramps and pain

fever

fatigue

rectal bleeding

loss of appetite

could impact joints, eyes, skin, liver

36
Q

complications of Crohn’s disease

A

obstruction due to swelling and formation of scar tissue.

development of fissures

abscesses

fistulas (abnormal tunnel between 2 structures)

37
Q

what is the valsalva maneuver

A

closure of the glottis, contraction of the abdominal and thoracic muscles causes transient increase in blood pressure. helps defecation.

38
Q

why is everyone supposed to be lactose intolerance but isn’t

A

we are genetically programmed to become lactose intolerant, but the body continues to produce lactase as long as we consume dairy products.

39
Q

what happens in lactose intolerance

A

lactose (normally digested in SI) is passed to large intestine where E coli breaks it down into monosaccharides. this causes large volumes of methane, H2 gas and lactic acic = flatus!!

flatus distension of the colon causes pain.

ecoli breaking into monosaccharides into FA which causes water movement into Li causing diarrhea.

40
Q

what causes diarrhea in lactose intolerance?

A

E coli breaks down lactose into FA which osmotically causes water movement into the LI

41
Q

what causes pain in lactose intolerance?

A

flatus distension of the colon

42
Q

what serum hormones regulate appetite

A

leptin, ghrelin, growth hormone, neuropeptide Y

43
Q

what secretes neuropeptide Y?

A

paraventricular nucleus of the hypothalamus

44
Q

what is the most abundant peptide of the CNS?

A

neuropeptide Y

45
Q

actions of neuropeptide Y

A
  1. most potent orexigenic peptide in the brain (increases food intake)
  2. increases proportion of energy stored as fat
  3. blocks nociceptive signals to the brain (pain)
  4. augments vasoconstrictor effects of noradrenergic neurons
46
Q

3 actions of ghrelin

A
  1. stimulation of growth hormone secretion
  2. increase hunger
  3. suppress fat utilization in adipose tissue

APPETITE REGULATING FACTOR

47
Q

how does ghrelin stimluate growth hormone secretion?

A

binds growth hormone secretagogue receptor (GHSR1a) in the anterior pituitary resulting in release of GH

48
Q

how does ghrelin increase hunger?

A
  1. acts on hypothalamic appetite regulation receptors
  2. hippocampal receptors and regions with reward systems
49
Q

what circuits does ghrelin activate?

A

some of the same circuits that are involved in drug reward

50
Q

what produces ghrelin?

A

P/D1 cells lining fundus of stomach

AND

epsilon cells of the pancreas

synthesize preprohormone then is proteolytically processed to yield 28-AA peptide when its in the right place

51
Q

generally, what does ghrelin stimluate

A

food intake, promotes body weight gain, and adipogenesis

52
Q

describe ghrelin levels before and after meals

A

ghrelin levels increase before meals and decrease after meals

53
Q

what produces leptin?

A

adipose tissue

54
Q

how does leptin provide satiety?

A

leptin binds to neuropeptide Y neurons in the arcuate nucleus so that it decreases the activity of the neuropeptide Y neurons. signals the brain that the body has had enough to eat.

55
Q

what is the most potent orexigenic peptide in the body

A

neuropeptide Y

56
Q

what 4 neuropeptides play essential roles in regulation of food intake and energy homeostasis?

A
  1. the agouti related protein (AgRP)
  2. neuropeptide Y (NP-Y)
  3. proopiomelanocortin (POMC)
  4. cocaine and amphetamine regulated transcript (CART)
57
Q

what is CART

cocaine and amphetamine regulated transcript

A

a neuropeptide that plays roles in reward, feeding, and stress that also serves as a NT

58
Q

what is POMC

proopriomelanocortin

A

a 241aa hormone precursor that cleaves in 8 places to give rise to 10 active compounds with roles in pain and energy homeostasis, melanocyte stimulation, and immune modulation

59
Q

what is one of the most potent and long lasting appetite stimulators in humans

A

AgRP (agouti related protein)

60
Q

how does ghrelin act on the body

A
  1. is relased from P/D1 cells in fundus of stomach or epsilon cells in pancreas. acts on arcuate nucleus to make NP-T and AgRP coexpression. this leads to a strong orexigenic signal to the paraventricular nucleus in the hypothalamus to stimulate ultradian and rhythmic patterns
61
Q

what does leptin inhibit

A

leptin released by adipocytes inhibts arcuate nucleus (NP-Y and AgRP) AND ghrelin release by fundus of stomach

62
Q

how does leptin work on the body

A

released from adipocytes to activate POMC and CART cells in the arcuate nucleus to send anorexigenic negative signals to the paraventricular nucleus.

Medical Physiology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions