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Block 4: Endocrinology > second half > Flashcards

second half Flashcards

1
Q

adequate intake

A

level recommended for indv in particular life stage/gender group to be “adequate” when there is not enough data to set an RDA

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2
Q

estimate avg req

A

value estimated to meet req in 50% of apparently healthy indv in particular life stage and gender group

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3
Q

recommended daily allowance

A

estimate of avg daily nutrient level intake req to meet 97-98% US pop EAR + 2SD

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4
Q

tolerated upper intake level

A

highest average of daily nutrient intake that poses no adverse risk to healthy indv in pop

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5
Q

water soluble vitamins

A

ascorbic acid (vit C) B1 B2 B3 Biotin Panthothenic acid Folic acid B12 B6 =pyridoxine pyridoxal pyridoxamine

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6
Q

fat solute vitamins

A

ADEK

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7
Q

What reaction is biotin a cofactor in

A

acetyl co A to malonyl co A Pyruvate to OAA propionyl co A to methylmalonyl co a

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8
Q

What is B12 a cofactor in

A

methylmalonyl CoA –> succinylcholine Co A homocysteine to Ile/Met/Val/Thr

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9
Q

B1 name

A

Thiamine Cofactor = thiamine pyrophosphate

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10
Q

B2 name

A

Riboflavin Cofactor = FMN, FAD

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11
Q

B3 name

A

Niacin Cofactor = NAD+, NADP+

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12
Q

B5 name

A

Panthothenic acid Cofactor = coenzyme A

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13
Q

B6 name

A

Pyridoxine, pyridoxal, pyridoxine Cofactor = PLP (Pyridoxal phosphate)

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14
Q

B7 name

A

Biotin

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15
Q

B9 name

A

Folic acid Cofactor = tetrahydrofolate

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16
Q

B12 name

A

Cobalamin Cofactor = deoxyadenosyl cobalamin, methyl cobalamin)

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17
Q

B vitamins

A

water soluble; deficiencies can result from diet, defective uptake, drug interactions supplementation neither necessary nor useful for average adult

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18
Q

B1

A

Thiamine

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19
Q

TPP

A

what thiamine is converted to; serves as cofactor for oxidative decarboxylation reactions for ENERGY PRODUCTION

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20
Q

Beriberi

A

B1 deficiency

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21
Q

Wernicke-Korsakoff Syndrome

A

B1 deficiency

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22
Q

which vitamins have toxicity/UL?

A

B3 (niacin), B6 (pyridoxine, pyridoxal, pyridoxine), vitamin E Folate and Vit C has UL but not toxicity

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23
Q

Pellagra

A

B3 (niacin/nicotinaminde) deficiency; diarrhea, dermatitis, dementia, death

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24
Q

isoniazid TB treatment

A

can cause B3 (niacin, nicotinamide) deficiency

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25
Q

avidin

A

protein found in egg whites that prevents the absorption of biotin and can lead to a biotin deficiency

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26
Q

genetic holocarboyxlase synthetase deficiency

A

ineffective use of biotin and can lead to biotin deficiency

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27
Q

megaloblastic anemia

A

anemia in which the RBCs don’t have the ability to divide because of shortage of nucleic acids; results from folate deficiency, because folate is necessary for the generation of nucleic acids

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28
Q

spina bifida

A

neural tube defects resulting from folate deficiency in early pregnancy

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29
Q

a-tocopherol

A

vitamin E

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30
Q

hephaestin

A

oxidizes exported Fe+2 to Fe+3, which can then be bound to transferrin

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31
Q

transferrin

A

binds Fe+3 in the blood

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32
Q

Hepcidin

A

stimulated by IL-6; serves to decrease Fe serum levels

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33
Q

incomplete proteins

A

plant proteins that are deficient in an essential amino acid corn beans

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34
Q

acceptable macronutrient distribution ranges

A

protein 10-35% fat 20-35% carbohydrate 46-65%

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35
Q

complete proteins

A

includes adequate levels of all esssential amino acids

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36
Q

how to determine N excretion

A

24h urinary urea nitrogen + 4g (feces, sweat etc)

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37
Q

positive nitrogen balance

A

indicates anabolic state , overall GAIN in body protein

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38
Q

negative nitrogen balance

A

indicates catabolic state, loss of body protein

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39
Q

nitrogen balance in pregnancy

A

positive

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40
Q

low quality protein diet

A

negative

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41
Q

sepsis

A

negative hyper catabolic state!

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42
Q

total daily energy expenditure

A

BMR + physical activity + energy used for digestion and storage of food

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43
Q

states that increase BMR

A

pregnancy fever hyperthyroidism

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44
Q

states that decrease BMR

A

aging (lose muscle) starvation hypothyroidism

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45
Q

thermic effect of feeding

A

work of digestion, approx 5-10% total energy expenditure

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46
Q

BMI

A

weight/height^2 (kg/m^2) the ratio of weight to height weight (lbs) x 703 / height in inches ^2

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47
Q

what are the categories for BMI

A

underweight, normal, overweight, obese

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48
Q

What is the goal of CCK?

A

to promote fat digestion and absorption

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49
Q

What substances stimulate HCl secretion?

A

Histamine

ACh

Gastrin

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50
Q

What substances inhibit HCl secretion

A

somatostatin

low pH

prostaglandins

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51
Q

zymogen granules

A

where pancreatic enzymes are stored until a stimulus tells them to be secreted

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52
Q

what might stimulate zymogen granules to secrete their contents

A

CCK or parasympathetic stimulation

recall: the goal of CCK is to promote fat digestion and absorption

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53
Q

Zollinger Ellison syndrome

A

gastrinoma, tumor secreting excess gastrin

gastrin stimulates HCl secretion by parietal cells in the stomach

therefore in this condition - see elevated HCl and elevated parietal cell mass

Tx: cimetidine and omeprazole, surgical resection

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54
Q

cimetidine

A

H2 receptor inhibitor

(therefore, end result is to decrease HCl secretion)

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55
Q

omeprazole

A

H/K ATPase inhibitor (therefore end result is to decrease HCl secretion)

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56
Q

extrinsic autonomic NS innervation of gut

A

Sympathetic = celiac, superior and inferior mesenteric, hypogastric

Parasympathetic = vagus and pelvic

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57
Q

postganglionic sympathetic of gut are…

A

adrenergic

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58
Q

post ganglionic parasympathetic of the gut are either…

A

cholinergic or peptinergic

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59
Q

vasovagal reflex

A

reflex in which both afferent and efferent limbs are contained in vagus nerve

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60
Q

What happens in the resection of gastric antrum

A

removal of G cells therefore H+ secretion, gastric mucosa atrophy

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61
Q
A
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62
Q

what kind of cells secrete pepsinogen

A

gastric chief cells

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63
Q

what happens to pepsin at a pH greater than 5

A

it is denatured and inactivated

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64
Q

is pepsin essential for protein digestion

A

no

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65
Q

pancreatic enzymes

A

pancreatic lipase

cholesterol ester hydrolase

phospholipase A2

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66
Q

post prandial hyperemia

A

increased splanchnic blood flow after a meal

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67
Q

vasoactive hormones

A

CCK

neurotensin

bradykinin

kallidin

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68
Q

what is the overall effect of the ENS in the reseting state

A

Overall inhibitory effect

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69
Q

what does chemical denervation do to ENS

A

blocks most ENS Na channels

this causes an increase in small bowel motor activity (Recall, at rest, ENS has an overall inhibitory fxn)

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70
Q

what stimulates short arc reflexes in the bowel and colon?

A

distention

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71
Q

what are the short arc reflexes in the bowel and colon?

A

segmentation and peristalsis (fxn to move chyme toward colon)

stimulated by distention

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72
Q

Entero-gastric reflex

A
  • stimulated by = acid, hypertonicity, over-distention
  • decreases stomach emptying
  • increases duodenal activity DISTAL to stimulus
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73
Q

gastro-colic reflex

A
  • filling of stomach increases distal motor activity; esp of colon
    • infant diapers must be changed soon after feeding
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74
Q

entero-enteric reflexes

A
  • increases motor activity distal to a distending or irritating stimulus WHILE decreasing proximal activity!
    • clears offending stimulus from bowel
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75
Q

whats another name for long arc reflexes

A

vasovagal

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76
Q

general pattern of vasovagal activity

A

distention and or irritation inhibits proximal motor activity and stimulate distal motor activity

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77
Q

cecal frenulae

A

two “lips” that flank the entrance of the ileum into the colon

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78
Q

what does the material in the terminal ileum consist of

A
  • fluids
  • electrolytes
  • nutrients
  • mucus
  • bacteria
  • poorly digested/indigestible substances
    • colon recovers most fluids, nutrients and electrolytes!!!
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79
Q

colonic motor activity

A
  1. segmentation
  2. mass peristalsis
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80
Q

what is the stimulus for defecation

A

increased intra-rectal pressures from incr vol (>18mmHg)

pelvo-pelvic nerve pathway via stimulation of adenosine sitmulating nerves!

IF intra-rectal pressure exceeds 55mmHg, defecation will occur no matter what

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81
Q

what are the two events involved in defecation

A
  1. stimulation of defecation reflex
    • contraction of distal colon and relaxation of internal anal sphincter
  2. changing the ano-rectal angle
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82
Q

defecation reflex

A

contraction of distal colon

relaxation of internal anal sphincter

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83
Q

is the internal anal sphincter contracted or relaxed between voidings?

A

between voidings the internal anal sphincter is CONTRACTED

colonic and rectal visceral SMC has low tonus

myogenic activity stimulates internal anal sphincter circular muscle to contract

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84
Q

what do spinal lesions have to do with pooping

A

if the lesion is in the upper spinal cord, patient can still defecate because the reflex is integrated at the lower cord level

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85
Q

pelvopelvic reflex

A

required for defecation

stimulus is that there are stretch receptors in the distal colon that sense the stretch

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86
Q

what is the mechanism by which the anal-rectal angle becomes more obtuse?

A

cessaton of efferent motor input to skeletal muscles

note: neuromuscular problems prevent inhibition and may result in constipation

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87
Q

fecal incontinence

A

loss of pelvic floor tone, makes nagle more obtuse, fecal incontinence

can strengthen pelvic floor muscles using kegel exercises

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88
Q

what nerve is involved in the voluntary modulation of defecation reflex

A

pudendal n.

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89
Q

constipation

A

inappropriate decrease from NORMAL frequency of defecation

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90
Q

what are some causes of constipation

A
  • starvation
  • dehydration
  • surgery
  • antiypertensive agents *** common
  • organic obstruction
  • psychogenic
  • autonomic neuropathy
  • laxative abuse
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91
Q

whats a common cause of constipation

A

antihypertensive agent

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92
Q

diarrhea

A

an inappropriate increase in fecal water content

93
Q

defecation requires participation of 2 major events which are?

A

1) defecation reflex = contraction of distal colon and relaxation of internal anal sphincter
2) change in the analrectal angle

94
Q

What is/ are the differences between the fed and empty small bowel motility patterns

A

1) Fed = incr duration of motor activity, and change in transition rate depending on food compositon (ie high fat decr transition rate)
2) Fasting = MMC = clean the debris

95
Q

the bowel mucosa contains three types of cells - what are they?

A

villus

goblet

crypt cells

96
Q

what are the three ways for amino acids to get into the hepatic portal circulation

A

brush boarder peptidases

separate transporters for amino acids

endocytosis of proteins and peptides (enterocytes and M cells)

97
Q

where does nutrient absorption primarily occur

A

jejunum

98
Q

what has the highest caloric density

A

lipids

99
Q

starch

A
  • chains of glucose moleucles
  • digestion begins with salivary alpha amylase
    • inactivation of saliary amylase is dependent on size of meal
  • small bowel digestion via pancreatic amylase
100
Q

What is starch hydrolyzed to

A
  • alpha limit dextrins = 30%
  • malto-oligo-saccharides = 70%
    • G2 = maltose
    • G3 = maltotriose
    • G4-G9
101
Q

malto-oligo saccharides

A

G4-G9

G2 = maltose

G3= maltotriose

made from the digestion of starch by alpha amylase (salivary and pancreatic)

102
Q

what are the brushboarder enzymes involved in starch digestion

A

dextrinase and glucoamylase

103
Q

how are glucose and glaactose absorbed by small bowel enterocytes?

A

luminal SGLT1-Na co-transport

basolateral GLUT2

104
Q

how is fructose absorbed into the enterocyte?

A

luminal GLUT5 carriers

then basolateral GLUT2

105
Q

trehalose

A

2 glucose molecules joined at the 1’-1’ molecules

106
Q

lactose

A

galactose and glucose

107
Q

sucrose

A

fructose with glucose

108
Q

where is vitamin C absorbed

A

ileum

109
Q

what are the sources of protein

A

exogenous = diet

endogenous = digestive enzymes and desquamated cells

110
Q

enterokinase

A
  • initiates activation of pancreatic enzymes
  • secreted by crypts of lieberkuhn
  • binds to brushborder
    • is freed via presence of bile salts
  • is activated by the presence of its substrate, trypsinogen
111
Q

3 absorptive mechanisms of luminal enterocyte

A
  1. brush border peptidase for oligopeptides
  2. aa specific transporters
  3. endocytosis of proteins and peptides
112
Q

system B0

A

System Bo is a sodium dependent neutral aa transporter that serves as a specific aa transporter on the luminal end of the enterocyte, contributing to the enterocyte absorptive mechanisms

Neutral aa = arginine, lysine, histadine

113
Q

basolateral enterocyte membrane

A

3 sodium indp transporters move aa out of enterocyte

2 sodium DEPENDENT transporters move aa back into enterocyte

why? because intestinal mucosa is being replaced every 18 or so hours

114
Q

What is net absorption of individual aa vs oligopeptides?

A

aa abosrption is LESS than oligopeptides

  1. luminal aa absorption depends on physical proximity
  2. oligopeptides have kinetic advantage over single aa
115
Q

what are the three key pancreatic enzymes

A

pancreatic lipase

cholesterol ester hydrolase

phospholipase A2

116
Q

what does bile do to pancreatic lipase

A

sterically hinders it; therefore pancrease must secrete pro-colipase and activate it to colipase

117
Q

pancreatic lipase

A

forms FFA and monoglycerides

118
Q

cholesterol ester hydrolase

A

paancreatic enzyme that produces cholesterol and glycerol

119
Q

phospholipase A2

A

produces lysolecithin and FFA

120
Q

what is the first enzyme that starts to break down fat

A

lingual lipase

121
Q

what can lack of bile salts lead to?

A

steatorrhea and avitaminosis

(due to inability to absorb dietary fat)

122
Q

Hartnup disease

A

inability to absorb non polar amino acids

especially, tryptophan

(CNS and skin disorders)

123
Q

cystinuria

A

lack of dibasic aa transporters causes elevated excretion of cysteine

124
Q

where is folic acid absorbed

A

via a speific OH exchanger in the jejunum

125
Q

hemachromatosis (siderosis)

A

too much iron

126
Q

two mechanisms of calcium absorption

A

paracellular = whole small bowel; calcium flows between cells through the tight juncitons to hepatic portal veins; primary mechanism during high dietary ca activity

transcellular = through cell, mainly in duodenum

primary mechanism during moderate to low dietary ca activity

127
Q

Why is calcitriol necessary for proper calcium absorption

A

has four key fxns on duodenal and jejunal enterocytes

  1. TRPV6 channels on apical mem
  2. Calbindin D
  3. basolateral Ca/H ATPase
  4. basolateral Na/Ca exchanger
128
Q

TRPV6

A

calcium channel on the apical membrane of duodenal and jejunal enterocytes

129
Q

calbindin

A

binds calcium in the enterocyte

activated by calcitriol

causes incr in calcium absorption bc makes conc grad seem low

130
Q

what does overall iron absorption depend on

A

fullness of iron stores

level of erythropoietic activity

amt dietary iron intake

131
Q

where is iron primarily absorbed

A

duodenum

therefore damaged duodenal mucosa may cause microcytic anemia

132
Q

what is the effect of calcium on DMT1

A

Calcium is a low affinity noncompetitive inhibitor that inhibits DMT-1

therefore high dietary calcium will impede iron absorption!!!

DMT 1 is responsible for bringing non heme iron into cell (divalent metal ion transporter)

133
Q

hephaestin

A

oxidizes ferrous to ferric in plasma

so tht ferric iron can be bound to transferrin (protein tranporter molecule)

134
Q

hepcidin

A

liver hormone released during high iron plasma or inflammation

fxn: down regulate DMT and inhibits ferroportin, fe release from macrophages

135
Q

where is the greatest fraction of HCO3 secretion located

A

duodenum (why- neutralize acidic chyme)

136
Q

beneficial activities of intesetinal flora

A
  • metabolism of indigestable carbs
  • conversion of primary to secondary bile acids
  • synthesis of
    • vit K
    • folate
    • biotin
    • thiamin
  • prevention of overgrowht of pathogenic bacteria
  • training immune system to only attack pathogens
137
Q

primary site of water absorption

A

jejunum

138
Q

where is Na/H process primarily

A

jejunum

therefore jejunum becomes primary site of HCO3 absorption

139
Q

what are two ways Cl- can leave the cell?

A

basolateral Cl- channel

apical Cl- channel (cystic fibrosis channel)

140
Q

engram

A

robust memory trace; the sensation of nausea and emesis form this as a protective measure

141
Q

what do chief cells secrete

A

pepsinogen

142
Q

what does delta cell secrete

A

somatostatin

143
Q

somatostatin

A

inhibits gastric acid secreiton

  • inhibits parietal cells
  • inhibits gastrin secreting cells
  • inhibits EC cells (histamine secretion)
144
Q

whts the most important stimulus for D cell stimulation

A

pH<2

145
Q

what does the enterogastric reflex effect

A

it inhibits the parietal and G cells

146
Q

name some things that breach the mucosal barrier of the stomach

A

NSAIDS (decr prostaglandin synthesis therefore decr mucosal secretion)

nicotine

ethanol

H Pylori

Bile

147
Q

why is the duodenal mucosal barrier less effective?

A

the duodenum is a sensor! Therefore, dont want a super thick barrier bc then it wouldnt be able to sense things; it needs to konw what the physcial and chemical nature is of the chyme that it receives.

THEREFORE, duodenal ulceration of duodenum compared to stomach is 3:1

148
Q

what are the two ways potassium can exit the ileal and colonic enterocytes?

A
  • aldosterone sensitive Apical K+ channel
    • recall that aldosterone increases sodium reuptake and kicks potassium out
  • basolateral K chanel
149
Q

how does water flow

A

paracellularly

150
Q

secretory diarrhea

A

hypercholremic, hypokalemia acidosis

H gets trapped inside cell which causes acidosis

151
Q

how do you know its secretory diarrhea

A

loss of IONS

152
Q

how do you know its osmotic diarrhea

A

loss of NON ELECTROLYTES

153
Q

stool osmotic gap

A

SOG = [290- (stool Na+ + stool K+)

normal = 100-150 mosm/Kg

secretory <100

osmotic>150

154
Q

what is the stool osmotic gap in secretory diarrhea?

A

SOG<100mosm/Kg

155
Q

what is the stool osmotic gap in osmotic diarrhea?

A

SOG>150mosm/Kg

156
Q

more sodium and potassium in the stool during ____ diarrhea

A

secretory

157
Q

what can increase in cAMP synthesis within crypt cause?

A

cAMP synthesis incr due to toxins can cause secretory diarrhea which will have <100 stool osmotic gap

158
Q

what is the only place where bicarb is reabsorbed

A

Jejunum

159
Q

what is the main site for folate Fe and Ca absorption

A

duodenum

160
Q

proton pump inhibitor

A

selective and IRREVERSIBLE

block apical H/K proton pump

161
Q

H2 receptor antagonists

A

competitive REVERSIBLE inhibitor

blocks H2 receptor on parietal cell, thereby preventing histamine (from ECL cell) from being able to stimulate parietal cell acid secretion

162
Q

at what week does gut herniate into umbilical cord

A

week 6

90 degrees counterclockwise

163
Q

when does intestinal folds return to abdominal cavity

A

week 10

180 degrees counterclockwise

164
Q

hypospadias

A

due to failure of urethral folds to fuse; abnormal opening of penile urethra on ventral surface of penis

165
Q
A
166
Q

what does pineal gland produce?

A

melatonin

167
Q

what kind of neurons respond to increased temp

A

sympathetic cholinerginc neurons (Acting on sweat glands and cutaneous blood vessels–>vasodilation)

168
Q

what kind of neurons respond to decr temp

A

motor neurons (shivering)

Sympathetic adrenergic neurons

169
Q

how often does the entire epidermis renew?

A

every 15-30 days

170
Q

what is the only layer of the skin with cells that undergo mitosis?

A

St. Basale (“germanitiro”)

171
Q

langerhans cells

A

immune cells responsible for trapping antigens

172
Q

what are the four types of cells in the epidermis

A

Merkel

Langerhans

keratinocytes

melanocytes

173
Q

what aa is melanin derived from?

A

tyrosine

174
Q

what enzyme is involved in melanin produciton

A

tyrosinase

175
Q

Lysyl oxidase

A

required for the crosslinking of collagen and elastin; dependent on COPPER

(Marfans symptoms are the symptoms that you would also have with significnat copper deficiency)

176
Q

what is vitamin C’s effect on vitamin E

A

restores vitamin E to antioxidant form

177
Q

heme oxygenase

A

in the cytoplasm of the enterocyte, releases iron from heme

178
Q

heme transporter

A

transports heme into enterocyte

179
Q

hephaestin

A

oxidizes expored ferrous iron to ferric iron

180
Q

describe biofilm of infection

A

tend to be polymicrobial

  • neutrophils/macrophages cant engulf
  • further tissue damage from innate immune cells
  • resistance
  • matrix can impede antibiotic penetratio
181
Q

phosphodiesterase

A

inactivates cAMP

182
Q

what are the two types of tyrosine kinases

A

receptor associated tyrosine kinases

receptor tyrosine kinases

183
Q

what is anterior pituitary derived from

A

primitive foregut (ectoderm)

184
Q

contraindications to breastfeeding

A

HIV

Human T cell lymphotropic virus

active brucellosis

active untreated tuberculosis

active herpes varicella zoster

alcohol/drug abuse

ebola

galactosemia

185
Q

whats the bfd abt DHEA in the fetus

A

it is INERT! it prevents virilization of the fetus; it doesnt bind to either the androgen or the estrogen receptor

186
Q

what cell type makes antimullerian hormone

A

sertoli cells of the testes; responsible for causing the mullerian duct to degenerate

187
Q

what cell is responsible for phagocytosin germ cell cytoplasm

A

sertoli cell

188
Q

protamine

A

sperm version of histones; compacts DNA very tightly to protect it; involved in the remodeling phase that turns early spermatid into late spermatid

189
Q

chromaffin cell

A

post ganglionic sympathetic neuron; contain epinephrine or noepinephrine

190
Q

what kind of capillary in the thyroid?

A

fenestrated

191
Q

helicine arteries

A

dilate in erection

192
Q

what are the acrocentric autosomes

A

13,14,15,21,22

193
Q

cyp21 deficiency

A

hypotension

194
Q

cyp11 deficiency

A

hypertension

becasue 11DOC has mineralocorticoid

195
Q

lacunae

A

space where spiral arteries once were; created by proteases released by the syncytrotrophoblast

196
Q

hyaluronidase

A

released from acrosome; dissolves intercellular material btwn granulosa cells of corona radiata

197
Q

acrosin

A

facilitates penetration of zona by the sperm head

198
Q

what deficiency will have elevated mma

A

b12 deficiency

199
Q

what cells secrete intrinsic factor

A

parietal cells

(necessary for b12 absorption)

200
Q

what is r factor and where does it come from

A

comes from saliva; allows for absorption of B12

201
Q

where does primary saliva come from

A

acinar secretioin

202
Q

what is special about secondary saliva

A

hypotonic; derived from striated duct

203
Q

where is saliva from in basal secretion

A

low flow; submaxillary gland

204
Q

where is saliva coming from in high flow

A

comes from parotid gland (All serous, very watery, high pH)

205
Q

what kind of control is salivaiton under

A

NEURAL

206
Q

what phase gives most salivation

A

oral

207
Q

vagotomy and swallowing

A

decr solid swallow

incr liquid swallow

208
Q

what mediates mmc

A

motilin

209
Q

vagotomy

A

reduces antral motor activity and loss of receptive relaxation

increase in tonus!

210
Q

what kinds of cells release cck

A

i cells

211
Q

chemreceptor trigger zone

A

CTZ acts as second level of receptors that supplement emetic center

stimulated by meningitis, spoiled food, drugs, hypoxia, etc

212
Q

what does somatostatin bind to

A

recall - somatostatins goal is to decr hcl; it is released by D cells

binds to Gi receptor on parietal cell to decr cAMP

binds to receptor on EC cell to block histamine release

binds receptor on G cell to block gastrin release

213
Q

urease

A

how hpylori produces ammonia

214
Q

how does H pylori cause ulcers

A

cytotoxins break down mucosal barrier in stomac

inhibit SS secretion in D cells therefore incr h secretion

inhibits duodenal bicarb secretion

215
Q

where are deoxycholic and lithocolic acid made

A

made in the DUODENUM because they are secondary bile salts

216
Q

where are chenodeoxycholic and cholic acid made

A

liver because they are primary bile salts

217
Q

how do you make bile salts water soluble?

A

you conjugate them with glycine and taurine in the liver

218
Q

kernicterus

A

excess unconjugated bilirubin in infant –> irreversible CNS damage

219
Q

what is the most important phase of pancreas secretion

A

intestinal (80%) stimulated by cck and secretin

220
Q

law of the intestine

A

frequency of BER greater in PROXIMAL portion of SI b/c there are less gap juncitons in distal SI

221
Q

unstirred water layer

A

hypotheticallayer of water over mucosa that impedes diffusion

THICKNESS is INVERSELY PROPORTIONAL to motility of bowel

222
Q

what prevents overflowing of the colon

A

ileo-cecal junction

223
Q

what kind of metabolism is enterokinase involved in

A

amino acid metabolism

recall: enterokinase is produced in crypts

224
Q

where is enterokinase produced

A

crypts

225
Q

what kind of water absorption predominates in digestive period

A

paracellular

226
Q

what kind of water absorption predominates in between meals

A

transcellularly

227
Q

is sodium coupled nutrient transport affect by bacterial toxins?

A

no. in fact, this is how most na in the jejunum is absorbed and water follows paracellularly; secretory diarrhea (<100SO, secretion of ions) can be overcome by ingestion of nutrient containing water

228
Q

where are leaky tight junctions found

A

duodenum and jejunum; thats why the sodium electrogenic transport only works in ileum and colon, because those are the only places that can establish an electric potential

229
Q

stool osmotic gap

A

normal = 100-150

calculated via: 290 - (Na+K in stool)

<100 - secretory

>150 - osmotic

Block 4: Endocrinology (4 decks)

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