FINAL HELP lol Flashcards
AGRP + NP Y
POMC + MSH
effect on food and EE
AGRP= increase food intake decrease energy expenditure
POMC= increase energy, decrease food
where are AGRP and POMC found
ACN and PVN arcuate nucleus and paraventricular nucleus
what effect does serotonin have on MSH/POMC
increase it which decrease food intake and increase EE
what happens to beta cells in bad pancreas obese situation
apoptosis or turn to alpha cells and secrete glucagon
what is bile acids made from
made from cholesterol in hepatocytes and stored in gallbladder
primary and secondary bile acids
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
where are magnocellular in hypothalamus and where does go to
SON and PVN supraoptic and paraventricular
go to posterior pituitary
GH pathway
GHrH –> GH –> IGF-1
stimulators of GH
GHRH, ghrelin, dopamine, catecholamines, arginine, hypoglycemia
inhibitors of GH
somatostatin/GHIH, hyperglycemia, IGF-1
GHIH:
-g alpha –>tyrosine phosphates
-K+ hyper polarize
type of receptor for GH
class 1 cytokine
acromegaly and gigantism
acromegaly: somatotrope adenoma; over secrete GH
gigantism: increase GH before epiphyseal long bone closure
prolactin inhibtor
dopamine
prolactin stimualtors
suckling, estrogen, GnRH, prolactin releasing factors (TRH, oxytocin, vasoactive intestinal peptide)
glucocorticoids, mineralocorticoid and androgens zona??
glucocorticoids- cortisol – zona fasiculata
mineralocorticoids - aldosterone — zone glomerulosa
androgen in zona reticularis
where is adrenal cortex derived from
where is adrenal medulla derived from
cortex is mesoderm
medulla is neural crest cells (“SNS”) which become chromaffin cells
catecholamines
NE and Ea
aldosterone stimualtor
K+
angiotensin II
weakly ACTH
what are the adrenals bood supply
suprarenal artery and vein
what are steroid hormones made from
cholesterol
pathway to make cortisol
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
cholesterol esters into cholesterol via
cholesterol ester hydrolase
PKA helps cholesterol into inner mitochondrial matrix via
sTAR
cholesterol –> pregnenolone via
side chain cleavage enzyme
ACTH upregulated…
LDL receptors, CEH, sTAR, SCC enzymes
what impacts CRH and ACTH
circadian rhythm, SCN, melatonin
how is aldosterone synthesizes
same as glucocorticoids but when become corticosterone is then converted into aldosterone via aldosterone synthase
enzyme to get corticosterone into aldosterone
aldosterone synthase
RAAS
renin –> angiotensin –> angio I –> angio II –>
effects:
vasoconstriction
stimulate aldosterone
increase ADH
increase sodium absorption
secrete potassium
s
how are cortisol and aldosterone metabolized
glucoronidate in the liver
make the hydrophobic molecules more polar to be exerted in urine
what are aldosterone and cortisol secreted as in the urine
cortisol= 17 hydroxycorticosteroid
aldosterone = 18=glucoronide
what are catecholamines (NE and E) made from
tyrosine
what stimulate NE and E
SNS, ACTH, cortsol
how to make NE and E
tyrosine –> DOPA –> dopamine –> NE –> E
how to go from NE –> E
need cortisol and use of PMNT enzyme
how can acetylcholine cause exocytose NE and E
acetylcholine –> bind chromaffin cell –> Ca2+ influx –. exocytosis of NE and E
how to catabolize catecholamine to be excreted in urine
NE –> normetanephrine
E –> metanephrine
both via COMT
then turn normetanephrine and metanephirn in VMA (vamandelic acid) via MAO enzyme
then into urine
Cushings vs Addisons effect on adrenals and where they act
cushings= hypercortisolism
Cushing disease acts on pituitary
Addisons is primary and acts on adrenal gland and causes adrenocorticol insufficiency (hypo function)
is pheochromocytoma hypo or hyper function of adrenasl
hyper
tumor in chromaffin cells of adrenal medulla causing increase catecholamines
is congenital adrenal hyperplasia a hypo or hyperfunction
hypofunction
4 causes of excess cortisol seen in Cushing syndrome
- iatrogenic (most common)- exogenous glucocorticoids
- increase ACTH from hypothalamus or pituitary disease
- increase cortisol bc adenoma, carcinoma or nodular hyperplasia
- ectopic ACTH from paraneoplasm (non endocrine i.e. lung and renal)
in secondary arenocortical insufficiency what is the cause and what hormones are deficient
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.
what is cushing disease
seocondary
pituitary gland ahs ACTH producing microadenoma
primary cushing syndrom
adenoma at adrenal gland
what does dexamethasone do
inhibit ACTH at anterior pituitary
low dose dexamethasome;; effect on cortisol
healthy= suppress cortisol
cushing syndrome= no suppress
high dose dexamethose reason to use and effects on cushing disease and other
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
what is addision disease and what are the 4 causes
adrenal cortex destroyed (primary)
- TB
- AIDs
- autoimmune
- sarcoidosis or malignancy
2 types of autoimmune addison
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)
secondary adrenocorticol insufficiency? where? effects which hormeons
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)
in adrenal sufficiency if you give exogenous ACTH (cosyntropin) labs what are the results for primary/ Addison and secodndary adrenal insufficiency
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
primary hyperaldosteronsim is? what system is effected?
excess aldosterone secretion
suppresses RAAS
secondary hyperaldosteronsim
what system is activated
RAAS activated –> release aldosterone
aldosterone: renin ratio ARR is low
primary vs secondary hyperaldosteronism effect on RAAS
primary- RAAS suppressed by the high aldosterone
secondary: the RAAS is activated which is causing the aldosterone relase
what is congenital adrenal hyperplasia? is cortisol low or high? androgens? aldosterone? what is the enzyme at play?
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)
classic: salt wasting and simple virilizing
non classic
types of congenital adrenal hyperplasia
salt wasting: completely no 21- hydroxylase enzyme, in babies
simple virilizing: some enzyme
non classic: some enzyme. later in life, mimic PCOS, most common
what lab for congenital adrenal hyperplasi
17 hydroxyprogesterone is high
]
progesterone not getting converted into cortisol bc deficient in 21-hydroxyalse
pheochromocytoma; cells effected? low or high hormone
tumor in chromaffin cells of adrenal medulla causes increase in NE and E
hypertension
embryo organs of anterior and posterior pituitary
anterior: rathe pouch (envagination roof of pharynx)
posterior: infundibular process (evaginate 3rd ventricle)
what has more oxytocin vs ADH in the posterior pituitary; PVN or SON
SON has more ADH than oxytocin
PVN has more oxytocin than ADH
what are the 2 receptors for ADH and what do they respond to and where are they found
- osmoreceptors: in hypothalamus and lamina terminalis respons to decreased osmolarity
- baroreceptors, in carotid arch, carotid sinus and atria; respond to low blood pressure or low blood volume
what does oxytocin do to eject milk or contract uterus
contraction of smooth muscle –> Gq –> Ca2+ –> myosin
stimulators and inhibitors of oxytocin
stim: estrogen, sucking
inhibit: GABA, NO, endogenous opioids, fever, stress
what does ADH do and what are the 2 receptors
ADH increases water reabsorption
V1 receptor: vasocontrict muscle and increase blood pressure
V2 receptors: kidneys for water reabsorption
most common type of adenoma in the pituitary»> lol? what hormone?
lactotroph adenoma: hyperprolactinemia
–> amenorrhea, galactorrhea, infertile
inhibits GnRH and inhibits gonad steroids
what is a functional vs non functional tumpr in the pituitary
what is most common effevted
functional: gigantism, acromegaly, hyperprolactinemia
non functional tumors: dont secrete hormones; hypopituitarism, hypothyroid, adrenal insufficiency
GH is most common hypo
GH>FSH>LH >TSH>ACTH
what is the thyroid made from in embryo
from endodermal lining of primitive phayrnx
descends via thyroglossal duct
wk 7 is done
what are parafollicular cells in the thyroid what do they secrete
c cells
secrete calcitonin for Ca2+ regualtion
ingredients to make thyroid hromone
tyrosine and iodine
MIT and DIT
MIT= 1 iodine at the C3 of tyrosine
DIT= iodine at c3 and c5 of tyrosine
t4 vs t3 vs rt3
t3; active; 1 mit, 1 dit
t4; deiodinate to become t3; 2 DIT
tyrosine on thyroglobulin
where is thyroglobulin
made in follicular cells (mitochondria then RER) and seceeted into colloid
endocytosis when release t3 and t4 into blood
what brings iodine into the follicular cell
Na+/I+ symporter
on basolateral membrane
use Na+/K+ ATPase to pump Na+ out bc need to go against gradietn
how to get iodine to apical side of follicular cell
pendrin aka Cl-/I- exchanger
cl- out and iodine in
what is pended syndrome
no pendrin cl/i- exchanger
causes goiter, hearing loss, hypothyroid (or normal)
iodine; where is it absorbed, stored and excreted
absurd in SI
store in thyroid and kidneys
excrete 80% in kidney and rest in bile
what is thyroid peroxidase TPO? what help is needed?
apical membrane protein
turn iodide into iodine radical
need DUOX2 (for H2O2)
what’s less tightly bound t3 or t4
t3
what stimulates endocytosis of t3/t
TSH stimualtes
lysosome hydrolyse thyroglobulin and release t3/t4
recycle MIT and DIT
what 3 transport proteins to get t3 t4 into the blood
- albumin: primary carrier, low affinity
- transthyretin
- thyroxine binding globulin (TBG): high affinity for T4
what is deiodination
when t4 reaches the target tissue needs to become t3
what are the 3 deiodinases? where are they found?
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)
what is selenium needed for
in deiodinases because of selenocysteine residues
what has lower affinity t4 or t3? what is less tightly bound
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
TSH receptor? type of receptor? pathway
GPCR; phospholipase C
-hypertrophy or goiter if overstimulated
TRH –> TSH –> T4
free t4 or bound t4
release pattern of TSH
pulsatile, peaks at midnight
hasimotos vs graves in thyroid conviditon
Hashimoto is hypothyroid
graves is thryoxicosis/ hyper
hypothryoid/ reduced thyroid function
autoimmune: hashimotos, subacute/dequervain
iodine deficiency and non toxic goiter
congenital hypothyroidism, hypopituitarism. hypothalamic disease
iatrogenic
hyperthyroid of thyrotoxicosis
graves disease
toxic multi nodule goiter
neoplams: follicular and papillary adenoma anda adenocarcinomas
medullary and anaplastic carcinoma
what cell type is damaged most in hashimotos
T cell damage mainly via cytotoxic T cells, not anti thyroid antibodies
findings of immune in hashimotos
lymph infiltration with germinal centres
myxdema in what condition
in hashimotos
its skin thickens with no pitting edema
cause of subaute/ dequervain thyroiditis
virus
subaute/ dequervain thyroiditis immune findings
neutrophil –>lymphocyte infiltration
multi nucleate giant cells
what does subaute/ dequervain thyroiditis mimic? what are symtpsm
neck pain, fever , inflammed
mimics pharyngitis
silent thyroiditsi
occur with underlying autoimmune thyroiditis
usually resolved in 12 weeks
no pain, no fever, no ESR
goiter in what type of conditions
hypothyroid and thyrotoxicosis
diffuse non-toxic goiter
cause?
symptoms?
iodine deficiency; increase TSH, decrease T4
thyroid function is usually ok (euthyroid)
mass effects: compress airway
myxoedema coma
long term hypothyroid PLUS infection (or hypoglycemias, trauma, stress, stroke, meds etc)
hypotension
what is the most common cause of thyrotoxicosis
graves
what stimulates TSH receptor in graves
TSH receptor stimulating immunoglobulins (TSIs) –> not responsive to negative feedback
findings in graves disease
opthalmopthy
dermopathy; orange plaques and finger clubbing
toxic multinodular goiter- what is being produced- effects on hormone levels?
autonomous production of t3 t4 without TSH
mild hyperthyroid, t4 normal, TSH low
toxic adenoma causes and findings
mutated TSH-R
mild thyrotoxicosis
thyroid storm cause
hyperthyroid PLUS acute illness
congenital hypothrydoid causes
can be transient bc cross placenta from mom but usually permanent
causes: TSH-R antibody, gland dysgenesis
thyroid neoplasms- most common
follicular adenoma
papillary carcinoma
drugs for thyroid problems; PTU vs methimaxxole
PTU: inhibits thyroid peroxidase and inhibits deiodination of T4 to T3
methi: inhibits TPO
levothyroxine
synthetic T4
radioactive iodine for?
thyroid cancers –<> destroys gland
coenzyme –> vitamin VIA
vitamin –> coenzyme VIA
phosphatase
kinase
what are antithaimine factors for B1/thiamin
sulphur dioxide
thiaminases
polyphenols (2 thiamines bound)
what neurotransmitter can cause nerve conduction issues if thiamin deficeinct
acetylcholine
which systems are effectred most by thiamin b1 deficiency
CNS and cardiovascular (brain and heart)
wenicke korsakoff
wet beri beri
dry beri beri
what vitamin deficient and symptosm
WK: CNS, memory
wet: CVD, heart failure ((WET = BLOOD!!)
dry: CNS, motor and sensory
thiamine defieicnt
what is the transketolase test for? which vitamin?
needs TDP cofactor
in the pentose phosphate pathway (PPP)
if deficient than it increases
vitamin b1/thaimin
which vitamins for CAC
b1, b2 , b3, b5
what is the beta oxidation steps (substrate and product) and some vitamins needed
fatty acyl coa –>acetyl coa
b2,3,5
heme synthesis takes what from CAC
succinyl coa
which vitamins for redox rxn
b2 and b3
which vitamins for antioxidant glutathione
b2 b3
which vitamins for ETC
b2, b3
need the FADH/FMN from B2 and the NADH from B3
complexes in the CAC
pyruvate –> acetyl coa vis PDH complex
alpha ketoglutarate –> succinyl coa via alpha ketoglutarate dehydrogenase
succinate –> fumavate via succinate dehydrogenase
how can acytl coa make ketones and cholesterol (cholesterol then into steroid hormones)
acetyl coa –> HMG coa –> ketones or cholesterol
decarboxylation vs carboxylation - which vitmains
de: b6
carb: b7
riboflavin/ b2 for which hormones/ neurotransmitter metabolism
monoamine metabolism; breakdown dopamine, NE, E
testing for B2 riboflavin
glutathione reductase enzyme
what is B3 /niacin deficient called
pellagra; 4 D’s
what food causes niacin b3 deficinet
corn
b3 niacin in the cori cycle/anaerobic via which enzyme
lactate dehydrogenase
which dehydogenases in CAC is niacin b3 needed for
all dehydrogenases expect succinate dehydrogenase (which is FADH2)
nicotinic acid- which enzyme for vasodilation
what drug blocks it
what syndrome can it help
- vasodilatory prostaglandin release via cyclooxeganase
COX inhibitor is aspirin/ NSAID
help raynauds
how does niacin b3 dissolve clots
which disease to help
increase fibrinolysis by increasing plasmin and decreasing fibrinogen
helps atherosclerosis
other nicotinic acid effects
increase HDL, decrease VLDL/LDL
increase histamine release (*PUD)
hyperglycemia (glycogenesis)
b5 aka
and what’s its coenzyme
pantothenic acid
CoA
what reaction types for b6/ pyridox
transamination (amino acid into alpha keto acid)
sulfhydration
decarboxylation
what amino acid does b6 create to help make NAD+
tryptophan
which neurotransmitters does B6 make and from what amino acids
tryptophan –> serotonin
tyrosine –> dopamine
glutamate –> gaba
b6 deficiency
depresses
seizures
microcyte anemia
inflammation
b6 in GNG (glucose from amino acids)
cys –> pyruvate
ala –> pyruvate
asp –> oxaloacetate
glucose alanine cycle for B6
which type of rxn
where in body
pyruvate –> alanine via transamination
in musclew and liver
how does b6 desaturate fatty acids? effects on body
linoleic acid –> gamma linoleic acid which is anti inflammatory
what does b6 help make cysteine from
serine and homocysteine
what vitamin is the tryptophan load test for
b6
what is the tryptophan load test
tryptophan –> NAD via the b6 coenzyme PLP
if no PLP then will have xanthurenic acid
what does b7/ biotin coenzyme have
co2 and lysine
what reaction type does b7 do
carboxylase (to absorb)`
how does b7 and b12 help to make succinyl coa
propionyl coa –> (Co2 from B7) –> methylmalonyl coa –> (b12 mehtyl) –> succinyl coa
what is b9 folate made out of
THF is made out of 4 H’s + polyglutamate + 1C
how to get the 4 Hs for THF
via B3 reductase
reaction types for b9/folate
methylate/ 1 c transfer
folate conversion; vitamins required
b2, b3, b6, b12
what does folate make DNA and what diseases from deficiency
purine and pryrimidine synthesis
cancer, spina bifida, megaloblastic anemia,
where is folate stored and bound to what
liver via folate binding proteins
how does folate travel from liver to blood to SI
polyglu in storage to trap and monoglu in blood
which amino acids does b9 folate make and via what transfer
homocysteine and methionine via CH3 transfer
why is it important to make methionine
become SAM; a methyl donor for choline, epinephrine, DNA
how does methyl folate become THF
and what amino acids are being made
what other vitamin is needed
CH3 transfer
need b12
to make homocysteine into methionine
what happens if no b12 for homocysteine to methionine
w
which enzyme / gene is implicated usually
methyl folate trap
MTHFR enzyme
folate is implicated in depression why
correlated to THB which makes dopamine and serotinin
2 types of b12 coenzyme
adenosylcobalamin and methylcobalaminw
what is methylcobalmin do
transfer methyl group for methyl folate to homocysteine –> methionine –> SAM
what is adenosyl cobalamin for? what rxn
propionyl coa (b7) –> methylmalonyl coa (b12) –> succinyl coa
what is the methylmalonic acid test for
b12 deficiency
bc adenosyl cobalamin to make methylmalonyl coa –> succinyl coa
what is b12 from food broken down by in stomach
pepsin and hcl
hypochoridia bad
what protein carries b12 from stomach to SI
r protein
in the duodenum what grabs b12 from r protein to then be absorbed in the ileum
IF
how is b12 endocytose
in enterocytes B12-IF-R receptor mediated endoxytosis
goes to tissues via transcobalamin II then endocytosed
b12 storage where and in what form
liver as adenosyl cobalamin
deficiency in b12 effects
pernicious anemia (megaloblastic)
neurological –> alzheimers
tests for b12 defiecny
methylmalonic acid
homocysteine
both increase if deficient
somatopleure vs splanchnopleure
somatopleure is body wall
splanchnopleure is gut wall
3 cavities of intraembryonic coeloem
pleural, peritoneal, pericardial cavities
where is foregut locates
what divides it from mouth
what divides it from abdomen
between heart and brain
oropharyngeal membrane divides from stomodeum (mouth)
septum transversum (central tendon of diaphragm) divides abdominal and thoracic cavity
what does the connection between the midgut and umbilical vesicles get reduced to
omphaloenteric (vitelline) duct
vitelline duct connects midgut to yolk sac
what does diaphragm seperate and what canals are present that are eventually closed
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
what are the 3 things the diaphragm is dervied from
2 pleuroperitoneal membranes
muscular components from c3-c5 somites
mesentery of the esophagus
what is congenital diaphragmatic hernia
abdominal organs herniate into thoracic cavity because muscle cells absent in an area
what are the serous membrane lines? what are they made from?
from mesoderm
line abdominal organs, lungs, heart
foregut 1
forget 2
midgut
hindgut
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
what is the stroma vs parenchyma for and where do they come from
endoderm: epithelial lining/ parenchyma (for function)\
visceral mesoderm: stroma (for structure)
blood supply of frogut
celiac trunk
structures of foregut
pharynx and respiratory systems
esophagus, stomach
duodenum
liver + bilary + pancreas
how is the esophagus divided from trachea
esophagotracheal septum
muscle type and innervation of the esophagus sections
upper 2/3 is striated muscle via vagus nerve
lower 1/3 is smooth muscle via celiac plexus
polyhydramnios seen in…
esophageal atreasia
tracheoesophageal fistula
pyloric stenosis
duodenal atresia
what is esophageal atresia
blind tube ending
tracheoesophagela fistula
abnormal connection btwen esopahus and trachea
which way does stomach turn
90 degrees clockwise around long axis
innervation ofs tomach
vagus nerve
dorsal side of stomach becomes and moves?
ventral side of stomach becomes and moves?
ventral- lesser curvature - move right
dorsal- greater curvature- move left
liver on what side of mesogastrium
ventral
what ligament to connect liver to ventral body wall
falciform ligament
where in mesogastrium does spleen form and what week
5th week forms in dorsal mesogastrium
what ligament connects spleen to sotmach
gastrolineal ligament connects it to left posterior side of stomach
pancreas from what mesogastrium
dorsal m
mesenteries create what?
bulge down of dorsal mesogastrium and form greater omentum
plyoric stenosis
food doesnt pass stomach
vomit, polyhydramnios
duodenum formed by what and what arterial supply
foregut and midgut
celiac and superior mesenteric arteries
how does duodenum become a retroperitoneal organ
rotates with stomach
what needs to get lumen obliterated in duodenum
recanalization
duodenal stenosis vs duodenal atresia
stenosis: partial occlusion
atresia: complete occlusion (polyhydramnios)
what are liver and bilary apparatus formed from
foregut
what does liver bud (hepatic diverticulum) form
liver, gallbladder and bilary duct system
what is the bile duct
narrowing connection between hepatic diverticulum and foregut
ventral outgrowth of liver bud cause
gall bladder and cystic duct
hepatic sinusoids
x
extra hepatic bilary atresia
bile ducts blocked
bifid gall bladder
2x of them
pancreas formed by
foregut
what causes pancreatic ducts
duodenum rotates
pancreatic ducts formed by dorsal and ventral buds fusing
annular pancreas? what other organ is compromised?
abnormal rotation
- ventral bud forms ring of pancreatic tissue around duodenum
compress and obstruct duodenum
midgut creates which structures
SI; most of duodenum
cecum, appendix, ascending colon, right 2/3 of transverse colon
where is midgut located
suspended to dorsal abdominal wall via elongated mesentery and superior mesenteric artery
midugt loop
projected into proximal umbilical cord
artery for midgut
superior mesenteric artery
midgut loop; what rates around waht
2 counter clockwise orations; 90 protrusion, 180 returning
around superior mesenteric artery
how is cecum and appendix divided
cecal diverticulum
congenital omphalocele
herniation of intestinal loops into proximal umbilical cord
gastroschisis
malformed anterior abdominal wall
–>protrude into amniotic cavitty
umbilical hernia
intestine through umbilicus
meckel (ill diverticulum)- what causes it? what does it mimic?
yolk sac remains and forms diverticulum
mimic appendicitis
viltelline cyst
x
umbilical fistula
vitelline duct remains: intestine and umbilicus communicate
hindgut - what is the artery
inferior mesenteric artery
what organs from the hindgut
left 1/3 transverse colon, sigmoid colon, rectum, superior anal canal
urinary bladder and urethra
descending colon becomes retroperitoneal
what is the cloaca
terminal dilated portion of hindgut
what divides the cloaca and cloacal membrane in 2
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
what is the anal canal composed of? what divides the 2 parts?
superior 2/3= hindgut
inferior 1/3 = proctodeum (anal pit)
divided by pectinate line
where are internal and external hemorrhoids? why is one painful?
superior 2/3= hindgut = internal hemorrhodis (mucus membrane - no pain receptors)
inferior 1/3 = proctodeum (anal pit) (skin- pain receptors)
congenital megacolon (hirschspring disease)
no autonomic ganglion cells in myenteric plexus
- no relaxation of colon segment - cant move stool forward - no rhythmic contraction
amniotic fluid
polyhdyramnios
oligohydramnios
