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BMS200 > FINAL HELP lol > Flashcards

FINAL HELP lol Flashcards

1
Q

AGRP + NP Y
POMC + MSH

effect on food and EE

A

AGRP= increase food intake decrease energy expenditure

POMC= increase energy, decrease food

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2
Q

where are AGRP and POMC found

A

ACN and PVN arcuate nucleus and paraventricular nucleus

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3
Q

what effect does serotonin have on MSH/POMC

A

increase it which decrease food intake and increase EE

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4
Q

what happens to beta cells in bad pancreas obese situation

A

apoptosis or turn to alpha cells and secrete glucagon

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5
Q

what is bile acids made from

A

made from cholesterol in hepatocytes and stored in gallbladder

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6
Q

primary and secondary bile acids

A

primary: colic acid and chenodeoxycholic acid

C’S ARE FIRST- COME FROM CHOLESTEROL

secondary: deoxycholic acid and lithocholic acid

primary via hydroxylate enzymes

and secondary via microbiota

in SI and food and CCK

reabsorb in LI

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7
Q

where are magnocellular in hypothalamus and where does go to

A

SON and PVN supraoptic and paraventricular

go to posterior pituitary

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8
Q

GH pathway

A

GHrH –> GH –> IGF-1

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9
Q

stimulators of GH

A

GHRH, ghrelin, dopamine, catecholamines, arginine, hypoglycemia

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10
Q

inhibitors of GH

A

somatostatin/GHIH, hyperglycemia, IGF-1

GHIH:
-g alpha –>tyrosine phosphates
-K+ hyper polarize

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11
Q

type of receptor for GH

A

class 1 cytokine

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12
Q

acromegaly and gigantism

A

acromegaly: somatotrope adenoma; over secrete GH

gigantism: increase GH before epiphyseal long bone closure

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13
Q

prolactin inhibtor

A

dopamine

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14
Q

prolactin stimualtors

A

suckling, estrogen, GnRH, prolactin releasing factors (TRH, oxytocin, vasoactive intestinal peptide)

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15
Q

glucocorticoids, mineralocorticoid and androgens zona??

A

glucocorticoids- cortisol – zona fasiculata

mineralocorticoids - aldosterone — zone glomerulosa

androgen in zona reticularis

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16
Q

where is adrenal cortex derived from

where is adrenal medulla derived from

A

cortex is mesoderm

medulla is neural crest cells (“SNS”) which become chromaffin cells

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17
Q

catecholamines

A

NE and Ea

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18
Q

aldosterone stimualtor

A

K+
angiotensin II

weakly ACTH

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19
Q

what are the adrenals bood supply

A

suprarenal artery and vein

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20
Q

what are steroid hormones made from

A

cholesterol

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21
Q

pathway to make cortisol

A

have ACTH –> alpha GPCR –> adenyl cycles –> cAMP –> PKA

at same time have exogenous LDL –> cholesterol esters (via cholesterol ester hydrolase) –> cholesterol

PKA stimulates release of cholesterol from fat droplets into the inner mitochondrial membrane via sTAR (steroidigenic acute regulatory protein)

cholesterol –> pregnenolone (via side chain cleavage enzyme - rate limiting step) –> into corticosterone or cortisol

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22
Q

cholesterol esters into cholesterol via

A

cholesterol ester hydrolase

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23
Q

PKA helps cholesterol into inner mitochondrial matrix via

A

sTAR

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24
Q

cholesterol –> pregnenolone via

A

side chain cleavage enzyme

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25
Q

ACTH upregulated…

A

LDL receptors, CEH, sTAR, SCC enzymes

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26
Q

what impacts CRH and ACTH

A

circadian rhythm, SCN, melatonin

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27
Q

how is aldosterone synthesizes

A

same as glucocorticoids but when become corticosterone is then converted into aldosterone via aldosterone synthase

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28
Q

enzyme to get corticosterone into aldosterone

A

aldosterone synthase

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29
Q

RAAS

A

renin –> angiotensin –> angio I –> angio II –>

effects:
vasoconstriction
stimulate aldosterone
increase ADH
increase sodium absorption
secrete potassium
s

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30
Q

how are cortisol and aldosterone metabolized

A

glucoronidate in the liver

make the hydrophobic molecules more polar to be exerted in urine

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31
Q

what are aldosterone and cortisol secreted as in the urine

A

cortisol= 17 hydroxycorticosteroid
aldosterone = 18=glucoronide

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32
Q

what are catecholamines (NE and E) made from

A

tyrosine

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33
Q

what stimulate NE and E

A

SNS, ACTH, cortsol

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34
Q

how to make NE and E

A

tyrosine –> DOPA –> dopamine –> NE –> E

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35
Q

how to go from NE –> E

A

need cortisol and use of PMNT enzyme

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36
Q

how can acetylcholine cause exocytose NE and E

A

acetylcholine –> bind chromaffin cell –> Ca2+ influx –. exocytosis of NE and E

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37
Q

how to catabolize catecholamine to be excreted in urine

A

NE –> normetanephrine
E –> metanephrine
both via COMT

then turn normetanephrine and metanephirn in VMA (vamandelic acid) via MAO enzyme

then into urine

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38
Q

Cushings vs Addisons effect on adrenals and where they act

A

cushings= hypercortisolism
Cushing disease acts on pituitary

Addisons is primary and acts on adrenal gland and causes adrenocorticol insufficiency (hypo function)

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39
Q

is pheochromocytoma hypo or hyper function of adrenasl

A

hyper

tumor in chromaffin cells of adrenal medulla causing increase catecholamines

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40
Q

is congenital adrenal hyperplasia a hypo or hyperfunction

A

hypofunction

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41
Q

4 causes of excess cortisol seen in Cushing syndrome

A
  1. iatrogenic (most common)- exogenous glucocorticoids
  2. increase ACTH from hypothalamus or pituitary disease
  3. increase cortisol bc adenoma, carcinoma or nodular hyperplasia
  4. ectopic ACTH from paraneoplasm (non endocrine i.e. lung and renal)
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42
Q

in secondary arenocortical insufficiency what is the cause and what hormones are deficient

A

metastatic cancer, infection, infarction, irradiation

deficient cortisol and androgen

normal aldosterone

In this condition, cortisol and adrenal androgens are deficient because ACTH stimulates their production in the adrenal cortex. However, aldosterone production is primarily regulated by other mechanisms, particularly the renin-angiotensin system and plasma potassium levels, rather than ACTH.

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43
Q

what is cushing disease

A

seocondary

pituitary gland ahs ACTH producing microadenoma

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44
Q

primary cushing syndrom

A

adenoma at adrenal gland

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45
Q

what does dexamethasone do

A

inhibit ACTH at anterior pituitary

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46
Q

low dose dexamethasome;; effect on cortisol

A

healthy= suppress cortisol
cushing syndrome= no suppress

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47
Q

high dose dexamethose reason to use and effects on cushing disease and other

A

see if its cushing disease or other Cushing syndrome

suppressed cortisol= cushing disease (effect pituitary; secondary)

no suppression- ectopic ACTH dependent ie. kidney or lung

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48
Q

what is addision disease and what are the 4 causes

A

adrenal cortex destroyed (primary)

  1. TB
  2. AIDs
  3. autoimmune
  4. sarcoidosis or malignancy
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49
Q

2 types of autoimmune addison

A

APS1: autosomal recessive, in kids

APS2: skin and dental findings , hyperpigmentation, more common, later in life, Na+ decrease, K+ increase

addisons is destroy adrenal cortex (primary)

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50
Q

secondary adrenocorticol insufficiency? where? effects which hormeons

A

hypothalamus or pituitary

decrease cortisol and androgen

no effect on aldosterone so no changes in sodium or potassiuim
(bc aldosterone is only weakly effected by ACTH)

no hyperpigmentation (like Addison/ primary adrenocorticol insufficient)

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51
Q

in adrenal sufficiency if you give exogenous ACTH (cosyntropin) labs what are the results for primary/ Addison and secodndary adrenal insufficiency

A

Addison- low cortisol, high ACTH (no negative feedback);; cortisol doesnt inscrease

secondary: low cortisol, low ACTH ;; cortisol increases when given ACTH bc the issue is in pituitary/hypothalamus

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52
Q

primary hyperaldosteronsim is? what system is effected?

A

excess aldosterone secretion

suppresses RAAS

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53
Q

secondary hyperaldosteronsim

what system is activated

A

RAAS activated –> release aldosterone

aldosterone: renin ratio ARR is low

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54
Q

primary vs secondary hyperaldosteronism effect on RAAS

A

primary- RAAS suppressed by the high aldosterone

secondary: the RAAS is activated which is causing the aldosterone relase

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55
Q

what is congenital adrenal hyperplasia? is cortisol low or high? androgens? aldosterone? what is the enzyme at play?

A

autosomal recessive
low or no cortisol bc the 21-hydroxylase enzyme is defieicnt (which turns progesterone into cortisol)

there’s an accumulation of progesterone

also low aldosterone (hyponatremia, hyperkalemia, hypotension) because need corticosterone to turn into aldosterone

androgen are high bc they compensate –> virilization (genitals)

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56
Q

classic: salt wasting and simple virilizing
non classic

types of congenital adrenal hyperplasia

A

salt wasting: completely no 21- hydroxylase enzyme, in babies

simple virilizing: some enzyme

non classic: some enzyme. later in life, mimic PCOS, most common

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57
Q

what lab for congenital adrenal hyperplasi

A

17 hydroxyprogesterone is high
]
progesterone not getting converted into cortisol bc deficient in 21-hydroxyalse

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58
Q

pheochromocytoma; cells effected? low or high hormone

A

tumor in chromaffin cells of adrenal medulla causes increase in NE and E

hypertension

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59
Q

embryo organs of anterior and posterior pituitary

A

anterior: rathe pouch (envagination roof of pharynx)

posterior: infundibular process (evaginate 3rd ventricle)

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60
Q

what has more oxytocin vs ADH in the posterior pituitary; PVN or SON

A

SON has more ADH than oxytocin

PVN has more oxytocin than ADH

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61
Q

what are the 2 receptors for ADH and what do they respond to and where are they found

A
  1. osmoreceptors: in hypothalamus and lamina terminalis respons to decreased osmolarity
  2. baroreceptors, in carotid arch, carotid sinus and atria; respond to low blood pressure or low blood volume
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62
Q

what does oxytocin do to eject milk or contract uterus

A

contraction of smooth muscle –> Gq –> Ca2+ –> myosin

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63
Q

stimulators and inhibitors of oxytocin

A

stim: estrogen, sucking

inhibit: GABA, NO, endogenous opioids, fever, stress

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64
Q

what does ADH do and what are the 2 receptors

A

ADH increases water reabsorption

V1 receptor: vasocontrict muscle and increase blood pressure

V2 receptors: kidneys for water reabsorption

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65
Q

most common type of adenoma in the pituitary»> lol? what hormone?

A

lactotroph adenoma: hyperprolactinemia
–> amenorrhea, galactorrhea, infertile

inhibits GnRH and inhibits gonad steroids

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66
Q

what is a functional vs non functional tumpr in the pituitary

what is most common effevted

A

functional: gigantism, acromegaly, hyperprolactinemia

non functional tumors: dont secrete hormones; hypopituitarism, hypothyroid, adrenal insufficiency

GH is most common hypo

GH>FSH>LH >TSH>ACTH

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67
Q

what is the thyroid made from in embryo

A

from endodermal lining of primitive phayrnx

descends via thyroglossal duct

wk 7 is done

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68
Q

what are parafollicular cells in the thyroid what do they secrete

A

c cells

secrete calcitonin for Ca2+ regualtion

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69
Q

ingredients to make thyroid hromone

A

tyrosine and iodine

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70
Q

MIT and DIT

A

MIT= 1 iodine at the C3 of tyrosine
DIT= iodine at c3 and c5 of tyrosine

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71
Q

t4 vs t3 vs rt3

A

t3; active; 1 mit, 1 dit

t4; deiodinate to become t3; 2 DIT

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72
Q

tyrosine on thyroglobulin

where is thyroglobulin

A

made in follicular cells (mitochondria then RER) and seceeted into colloid

endocytosis when release t3 and t4 into blood

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73
Q

what brings iodine into the follicular cell

A

Na+/I+ symporter

on basolateral membrane

use Na+/K+ ATPase to pump Na+ out bc need to go against gradietn

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74
Q

how to get iodine to apical side of follicular cell

A

pendrin aka Cl-/I- exchanger

cl- out and iodine in

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75
Q

what is pended syndrome

A

no pendrin cl/i- exchanger

causes goiter, hearing loss, hypothyroid (or normal)

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76
Q

iodine; where is it absorbed, stored and excreted

A

absurd in SI

store in thyroid and kidneys

excrete 80% in kidney and rest in bile

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77
Q

what is thyroid peroxidase TPO? what help is needed?

A

apical membrane protein
turn iodide into iodine radical

need DUOX2 (for H2O2)

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78
Q

what’s less tightly bound t3 or t4

A

t3

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79
Q

what stimulates endocytosis of t3/t

A

TSH stimualtes

lysosome hydrolyse thyroglobulin and release t3/t4

recycle MIT and DIT

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80
Q

what 3 transport proteins to get t3 t4 into the blood

A
  1. albumin: primary carrier, low affinity
  2. transthyretin
  3. thyroxine binding globulin (TBG): high affinity for T4
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81
Q

what is deiodination

A

when t4 reaches the target tissue needs to become t3

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82
Q

what are the 3 deiodinases? where are they found?

A

deidoinase 1: liver , kidney, thyroid, pituitary (T4–>T3)

D2: brain, pituitary, brown fat (T4 –> T3)

D3: brain, reproductive tissue (T4 –>rT3 or inactivate T3) (good for decrease metabolic activity ie.. stress or calorie restriction)

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83
Q

what is selenium needed for

A

in deiodinases because of selenocysteine residues

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84
Q

what has lower affinity t4 or t3? what is less tightly bound

A

T4 has lower affinity for thyroid hormone receptor

t3 less tightly bound

think that t3 is active and needs to get away from binding and get to the receptor to do its job

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85
Q

TSH receptor? type of receptor? pathway

A

GPCR; phospholipase C
-hypertrophy or goiter if overstimulated

TRH –> TSH –> T4

free t4 or bound t4

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86
Q

release pattern of TSH

A

pulsatile, peaks at midnight

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87
Q

hasimotos vs graves in thyroid conviditon

A

Hashimoto is hypothyroid

graves is thryoxicosis/ hyper

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88
Q

hypothryoid/ reduced thyroid function

A

autoimmune: hashimotos, subacute/dequervain

iodine deficiency and non toxic goiter

congenital hypothyroidism, hypopituitarism. hypothalamic disease

iatrogenic

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89
Q

hyperthyroid of thyrotoxicosis

A

graves disease

toxic multi nodule goiter

neoplams: follicular and papillary adenoma anda adenocarcinomas

medullary and anaplastic carcinoma

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90
Q

what cell type is damaged most in hashimotos

A

T cell damage mainly via cytotoxic T cells, not anti thyroid antibodies

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91
Q

findings of immune in hashimotos

A

lymph infiltration with germinal centres

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92
Q

myxdema in what condition

A

in hashimotos

its skin thickens with no pitting edema

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93
Q

cause of subaute/ dequervain thyroiditis

A

virus

94
Q

subaute/ dequervain thyroiditis immune findings

A

neutrophil –>lymphocyte infiltration

multi nucleate giant cells

95
Q

what does subaute/ dequervain thyroiditis mimic? what are symtpsm

A

neck pain, fever , inflammed

mimics pharyngitis

96
Q

silent thyroiditsi

A

occur with underlying autoimmune thyroiditis

usually resolved in 12 weeks

no pain, no fever, no ESR

97
Q

goiter in what type of conditions

A

hypothyroid and thyrotoxicosis

98
Q

diffuse non-toxic goiter
cause?
symptoms?

A

iodine deficiency; increase TSH, decrease T4

thyroid function is usually ok (euthyroid)

mass effects: compress airway

99
Q

myxoedema coma

A

long term hypothyroid PLUS infection (or hypoglycemias, trauma, stress, stroke, meds etc)

hypotension

100
Q

what is the most common cause of thyrotoxicosis

A

graves

101
Q

what stimulates TSH receptor in graves

A

TSH receptor stimulating immunoglobulins (TSIs) –> not responsive to negative feedback

102
Q

findings in graves disease

A

opthalmopthy
dermopathy; orange plaques and finger clubbing

103
Q

toxic multinodular goiter- what is being produced- effects on hormone levels?

A

autonomous production of t3 t4 without TSH

mild hyperthyroid, t4 normal, TSH low

104
Q

toxic adenoma causes and findings

A

mutated TSH-R

mild thyrotoxicosis

105
Q

thyroid storm cause

A

hyperthyroid PLUS acute illness

106
Q

congenital hypothrydoid causes

A

can be transient bc cross placenta from mom but usually permanent

causes: TSH-R antibody, gland dysgenesis

107
Q

thyroid neoplasms- most common

A

follicular adenoma

papillary carcinoma

108
Q

drugs for thyroid problems; PTU vs methimaxxole

A

PTU: inhibits thyroid peroxidase and inhibits deiodination of T4 to T3

methi: inhibits TPO

109
Q

levothyroxine

A

synthetic T4

110
Q

radioactive iodine for?

A

thyroid cancers –<> destroys gland

111
Q

coenzyme –> vitamin VIA

vitamin –> coenzyme VIA

A

phosphatase

kinase

112
Q

what are antithaimine factors for B1/thiamin

A

sulphur dioxide
thiaminases
polyphenols (2 thiamines bound)

113
Q

what neurotransmitter can cause nerve conduction issues if thiamin deficeinct

A

acetylcholine

114
Q

which systems are effectred most by thiamin b1 deficiency

A

CNS and cardiovascular (brain and heart)

115
Q

wenicke korsakoff
wet beri beri
dry beri beri

what vitamin deficient and symptosm

A

WK: CNS, memory
wet: CVD, heart failure ((WET = BLOOD!!)
dry: CNS, motor and sensory

thiamine defieicnt

116
Q

what is the transketolase test for? which vitamin?

A

needs TDP cofactor

in the pentose phosphate pathway (PPP)

if deficient than it increases

vitamin b1/thaimin

117
Q

which vitamins for CAC

A

b1, b2 , b3, b5

118
Q

what is the beta oxidation steps (substrate and product) and some vitamins needed

A

fatty acyl coa –>acetyl coa

b2,3,5

119
Q

heme synthesis takes what from CAC

A

succinyl coa

120
Q

which vitamins for redox rxn

A

b2 and b3

121
Q

which vitamins for antioxidant glutathione

A

b2 b3

122
Q

which vitamins for ETC

A

b2, b3

need the FADH/FMN from B2 and the NADH from B3

123
Q

complexes in the CAC

A

pyruvate –> acetyl coa vis PDH complex

alpha ketoglutarate –> succinyl coa via alpha ketoglutarate dehydrogenase

succinate –> fumavate via succinate dehydrogenase

124
Q

how can acytl coa make ketones and cholesterol (cholesterol then into steroid hormones)

A

acetyl coa –> HMG coa –> ketones or cholesterol

125
Q

decarboxylation vs carboxylation - which vitmains

A

de: b6

carb: b7

126
Q

riboflavin/ b2 for which hormones/ neurotransmitter metabolism

A

monoamine metabolism; breakdown dopamine, NE, E

127
Q

testing for B2 riboflavin

A

glutathione reductase enzyme

128
Q

what is B3 /niacin deficient called

A

pellagra; 4 D’s

129
Q

what food causes niacin b3 deficinet

A

corn

130
Q

b3 niacin in the cori cycle/anaerobic via which enzyme

A

lactate dehydrogenase

131
Q

which dehydogenases in CAC is niacin b3 needed for

A

all dehydrogenases expect succinate dehydrogenase (which is FADH2)

132
Q

nicotinic acid- which enzyme for vasodilation

what drug blocks it

what syndrome can it help

A
  1. vasodilatory prostaglandin release via cyclooxeganase

COX inhibitor is aspirin/ NSAID

help raynauds

133
Q

how does niacin b3 dissolve clots

which disease to help

A

increase fibrinolysis by increasing plasmin and decreasing fibrinogen

helps atherosclerosis

134
Q

other nicotinic acid effects

A

increase HDL, decrease VLDL/LDL

increase histamine release (*PUD)

hyperglycemia (glycogenesis)

135
Q

b5 aka

and what’s its coenzyme

A

pantothenic acid

CoA

136
Q

what reaction types for b6/ pyridox

A

transamination (amino acid into alpha keto acid)

sulfhydration

decarboxylation

137
Q

what amino acid does b6 create to help make NAD+

A

tryptophan

138
Q

which neurotransmitters does B6 make and from what amino acids

A

tryptophan –> serotonin
tyrosine –> dopamine
glutamate –> gaba

139
Q

b6 deficiency

A

depresses
seizures
microcyte anemia
inflammation

140
Q

b6 in GNG (glucose from amino acids)

A

cys –> pyruvate
ala –> pyruvate
asp –> oxaloacetate

141
Q

glucose alanine cycle for B6

which type of rxn

where in body

A

pyruvate –> alanine via transamination

in musclew and liver

142
Q

how does b6 desaturate fatty acids? effects on body

A

linoleic acid –> gamma linoleic acid which is anti inflammatory

143
Q

what does b6 help make cysteine from

A

serine and homocysteine

144
Q

what vitamin is the tryptophan load test for

A

b6

145
Q

what is the tryptophan load test

A

tryptophan –> NAD via the b6 coenzyme PLP

if no PLP then will have xanthurenic acid

146
Q

what does b7/ biotin coenzyme have

A

co2 and lysine

147
Q

what reaction type does b7 do

A

carboxylase (to absorb)`

148
Q

how does b7 and b12 help to make succinyl coa

A

propionyl coa –> (Co2 from B7) –> methylmalonyl coa –> (b12 mehtyl) –> succinyl coa

149
Q

what is b9 folate made out of

A

THF is made out of 4 H’s + polyglutamate + 1C

150
Q

how to get the 4 Hs for THF

A

via B3 reductase

151
Q

reaction types for b9/folate

A

methylate/ 1 c transfer

152
Q

folate conversion; vitamins required

A

b2, b3, b6, b12

153
Q

what does folate make DNA and what diseases from deficiency

A

purine and pryrimidine synthesis

cancer, spina bifida, megaloblastic anemia,

154
Q

where is folate stored and bound to what

A

liver via folate binding proteins

155
Q

how does folate travel from liver to blood to SI

A

polyglu in storage to trap and monoglu in blood

156
Q

which amino acids does b9 folate make and via what transfer

A

homocysteine and methionine via CH3 transfer

157
Q

why is it important to make methionine

A

become SAM; a methyl donor for choline, epinephrine, DNA

158
Q

how does methyl folate become THF

and what amino acids are being made

what other vitamin is needed

A

CH3 transfer

need b12

to make homocysteine into methionine

159
Q

what happens if no b12 for homocysteine to methionine
w
which enzyme / gene is implicated usually

A

methyl folate trap

MTHFR enzyme

160
Q

folate is implicated in depression why

A

correlated to THB which makes dopamine and serotinin

161
Q

2 types of b12 coenzyme

A

adenosylcobalamin and methylcobalaminw

162
Q

what is methylcobalmin do

A

transfer methyl group for methyl folate to homocysteine –> methionine –> SAM

163
Q

what is adenosyl cobalamin for? what rxn

A

propionyl coa (b7) –> methylmalonyl coa (b12) –> succinyl coa

164
Q

what is the methylmalonic acid test for

A

b12 deficiency

bc adenosyl cobalamin to make methylmalonyl coa –> succinyl coa

165
Q

what is b12 from food broken down by in stomach

A

pepsin and hcl

hypochoridia bad

166
Q

what protein carries b12 from stomach to SI

A

r protein

167
Q

in the duodenum what grabs b12 from r protein to then be absorbed in the ileum

A

IF

168
Q

how is b12 endocytose

A

in enterocytes B12-IF-R receptor mediated endoxytosis

goes to tissues via transcobalamin II then endocytosed

169
Q

b12 storage where and in what form

A

liver as adenosyl cobalamin

170
Q

deficiency in b12 effects

A

pernicious anemia (megaloblastic)

neurological –> alzheimers

171
Q

tests for b12 defiecny

A

methylmalonic acid
homocysteine

both increase if deficient

172
Q

somatopleure vs splanchnopleure

A

somatopleure is body wall
splanchnopleure is gut wall

173
Q

3 cavities of intraembryonic coeloem

A

pleural, peritoneal, pericardial cavities

174
Q

where is foregut locates

what divides it from mouth

what divides it from abdomen

A

between heart and brain

oropharyngeal membrane divides from stomodeum (mouth)

septum transversum (central tendon of diaphragm) divides abdominal and thoracic cavity

175
Q

what does the connection between the midgut and umbilical vesicles get reduced to

A

omphaloenteric (vitelline) duct

vitelline duct connects midgut to yolk sac

176
Q

what does diaphragm seperate and what canals are present that are eventually closed

A

septum transversum (central tendon of diaphragm) divides thoracic and abdominal cavity byut has pericardiopertoneal canals

these canals are closed by pleuroperioneal folds creating pleural and peritoneal cavitiies

177
Q

what are the 3 things the diaphragm is dervied from

A

2 pleuroperitoneal membranes

muscular components from c3-c5 somites

mesentery of the esophagus

178
Q

what is congenital diaphragmatic hernia

A

abdominal organs herniate into thoracic cavity because muscle cells absent in an area

179
Q

what are the serous membrane lines? what are they made from?

A

from mesoderm

line abdominal organs, lungs, heart

180
Q

foregut 1
forget 2
midgut
hindgut

A

foregut 1: pharynx to respiratory diverticulum

foregut 2: below phayrnx to liver

midgut: below liver to right 2/3 and left 1/3 of transverse colon

hingut: left 1/3 transverse colon and cloacal memrbane

181
Q

what is the stroma vs parenchyma for and where do they come from

A

endoderm: epithelial lining/ parenchyma (for function)\

visceral mesoderm: stroma (for structure)

182
Q

blood supply of frogut

A

celiac trunk

183
Q

structures of foregut

A

pharynx and respiratory systems

esophagus, stomach

duodenum

liver + bilary + pancreas

184
Q

how is the esophagus divided from trachea

A

esophagotracheal septum

185
Q

muscle type and innervation of the esophagus sections

A

upper 2/3 is striated muscle via vagus nerve

lower 1/3 is smooth muscle via celiac plexus

186
Q

polyhydramnios seen in…

A

esophageal atreasia

tracheoesophageal fistula

pyloric stenosis

duodenal atresia

187
Q

what is esophageal atresia

A

blind tube ending

188
Q

tracheoesophagela fistula

A

abnormal connection btwen esopahus and trachea

189
Q

which way does stomach turn

A

90 degrees clockwise around long axis

190
Q

innervation ofs tomach

A

vagus nerve

191
Q

dorsal side of stomach becomes and moves?

ventral side of stomach becomes and moves?

A

ventral- lesser curvature - move right

dorsal- greater curvature- move left

192
Q

liver on what side of mesogastrium

A

ventral

193
Q

what ligament to connect liver to ventral body wall

A

falciform ligament

194
Q

where in mesogastrium does spleen form and what week

A

5th week forms in dorsal mesogastrium

195
Q

what ligament connects spleen to sotmach

A

gastrolineal ligament connects it to left posterior side of stomach

196
Q

pancreas from what mesogastrium

A

dorsal m

197
Q

mesenteries create what?

A

bulge down of dorsal mesogastrium and form greater omentum

198
Q

plyoric stenosis

A

food doesnt pass stomach

vomit, polyhydramnios

199
Q

duodenum formed by what and what arterial supply

A

foregut and midgut

celiac and superior mesenteric arteries

200
Q

how does duodenum become a retroperitoneal organ

A

rotates with stomach

201
Q

what needs to get lumen obliterated in duodenum

A

recanalization

202
Q

duodenal stenosis vs duodenal atresia

A

stenosis: partial occlusion

atresia: complete occlusion (polyhydramnios)

203
Q

what are liver and bilary apparatus formed from

A

foregut

204
Q

what does liver bud (hepatic diverticulum) form

A

liver, gallbladder and bilary duct system

205
Q

what is the bile duct

A

narrowing connection between hepatic diverticulum and foregut

206
Q

ventral outgrowth of liver bud cause

A

gall bladder and cystic duct

207
Q

hepatic sinusoids

A

x

208
Q

extra hepatic bilary atresia

A

bile ducts blocked

209
Q

bifid gall bladder

A

2x of them

210
Q

pancreas formed by

A

foregut

211
Q

what causes pancreatic ducts

A

duodenum rotates

pancreatic ducts formed by dorsal and ventral buds fusing

212
Q

annular pancreas? what other organ is compromised?

A

abnormal rotation
- ventral bud forms ring of pancreatic tissue around duodenum

compress and obstruct duodenum

213
Q

midgut creates which structures

A

SI; most of duodenum

cecum, appendix, ascending colon, right 2/3 of transverse colon

214
Q

where is midgut located

A

suspended to dorsal abdominal wall via elongated mesentery and superior mesenteric artery

midugt loop

projected into proximal umbilical cord

215
Q

artery for midgut

A

superior mesenteric artery

216
Q

midgut loop; what rates around waht

A

2 counter clockwise orations; 90 protrusion, 180 returning

around superior mesenteric artery

217
Q

how is cecum and appendix divided

A

cecal diverticulum

218
Q

congenital omphalocele

A

herniation of intestinal loops into proximal umbilical cord

219
Q

gastroschisis

A

malformed anterior abdominal wall
–>protrude into amniotic cavitty

220
Q

umbilical hernia

A

intestine through umbilicus

221
Q

meckel (ill diverticulum)- what causes it? what does it mimic?

A

yolk sac remains and forms diverticulum

mimic appendicitis

222
Q

viltelline cyst

A

x

223
Q

umbilical fistula

A

vitelline duct remains: intestine and umbilicus communicate

224
Q

hindgut - what is the artery

A

inferior mesenteric artery

225
Q

what organs from the hindgut

A

left 1/3 transverse colon, sigmoid colon, rectum, superior anal canal

urinary bladder and urethra

descending colon becomes retroperitoneal

226
Q

what is the cloaca

A

terminal dilated portion of hindgut

227
Q

what divides the cloaca and cloacal membrane in 2

A

urorectal septum divided cloaca in 2
ventral: urogenital sinus
dorsal: rectum and upper anal canal

urorectal septum divides cloacal membrane in 2
-ventral urogenital membrane
-dorsal anal membrane

228
Q

what is the anal canal composed of? what divides the 2 parts?

A

superior 2/3= hindgut

inferior 1/3 = proctodeum (anal pit)

divided by pectinate line

229
Q

where are internal and external hemorrhoids? why is one painful?

A

superior 2/3= hindgut = internal hemorrhodis (mucus membrane - no pain receptors)

inferior 1/3 = proctodeum (anal pit) (skin- pain receptors)

230
Q

congenital megacolon (hirschspring disease)

A

no autonomic ganglion cells in myenteric plexus
- no relaxation of colon segment - cant move stool forward - no rhythmic contraction

231
Q

amniotic fluid

A

polyhdyramnios
oligohydramnios

BMS200 (40 decks)

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