Things I struggle with Part 2 Flashcards
what two anterior pituitary hormones are derivatives of POMC
ACTH and MSH
what are the anterior pit hormones with the same alpha subunit
TSH, LH, FSH, hCG
what does the beta subunit of a hormone determine
it determines the hormone specificity
what hormone is secreted from the intermediate lobe of the pit
MSH
what is the anterior pit derived from
rathkes pouch which is oral ectoderm
what is the posterior pit derived from
neuroectoderm
what are the alpha cells, beta cells, and delta cells of the pancreas and where are they located within the pancreatic buds
alpha- glucagon- peripheral
beta- insulin- central
somatostatin- interspersed
what are the effects of glucagon
it does glycogenolysis, and gluconeogenesis, and lipolysis and ketone production
what regulated glucagon secretion and what suppresses it
it is secreted in response to hypoglycemia, and it is inhibited by insulin, hyperglycemia, and somatistatin
what is the antagonist of prolactin
dopamine
tesamorelin- what does it do
it increases GH and is used for AIDs lipodystrophy
what does increased prolactin decrease
GNRH so FSH AND LH
what does tonic GNRH do
it surpasses the HPG axis
what does pulsatile GnRH do
it leads to puberty and fertility
what are somatostatin analogs used to treat
GI bleeding and acromegaly
what does TRH increase
prolactin and TSH
prolactin function
increases milk production and stops ovulation by decreasing the GnRH production
what can first or second degree hypothyroidism do to prolactin
it can increase prolactin because of the increase in TRH
what does bromocriptine do to prolactin
it decreases the production because it increases the DA
what does antipsychotics and OCP and Pregnancy do to prolactin
it increases the prolactin because of the decrease of dopamine
what is the function of GH
it stimulates linear and bulky growth through the stimulation of production of IGF-1 by the liver
what can excess IGF1 lead to
it can cause gigantism but it leads to insulin resistance
when is there increased secretion of GH
exercise, deep sleep, puberty, and hypoglycemia
when is there decreased secretion of GH
from glucose of r somatostatin
ghrelin function
stimulates hunger and GH and is released from the stomach
what increases ghrelin
Prader Willi or sleep deprivation
function of leptin
satiety hormone
what decreases leptin
decreased sleep or starvation
what does a mutation in the leptin gene do
congenital obesity
what does leptin do to the lateral thalamic nucelus
it inhibits it, which if there is a lesion then there is anorexia
what does leptin do to the ventromedial thalamic nucelus
it stimulates it so if there is a lesion then there is hyperphagia
endocannabanoid function
act at hypothalamus and nucleus accumbent to increase hunger
where is ADH from in the thalamus
supraoptic nuclues
what is the function of ADH
it regulates osmolaitity and bp. increases urine osm and decreases blood osm
which receptors are for serum osmolality
V2
which receptors are for BP regulation by ADH
V1
where does ADH act specifically in the kidney
CT it adds aquaporins to rescue water
what happens to the ADH level in central DI and nephrogenic DI
in central DI there is decreased ADH and in nephrogenic theres increased ADH
what can cause neprhogenic DI
Lithium blocking aquaporins or mutation in V2 receptor
desmopressin acetate- use
ADH analog for treatment of central DI and nocturnal enuresis
what regulates ADH
osmoreceptors and hypovolemia
cortisol functions
increase blood pressure, insulin resistance, gluconeogenesis, lipolysis, proteolysis, decreased fibroblast activity (striae), decreased inflammatory and immune responses- inhibit neutrophil adhersion, blocks histamine, reduces eosinophils, blocked IL2 production, inhibits leukotrienes and prostaglandins, decreased bone formation
how does cortisol increase BP
increased alpha 1 receipts on the arterioles which increases the sensitivity to NE and epi
at very high concentrations what other receptors can cortisol stimulate
aldosterone receptors
why can cortisol reactivate TB
it blocks IL2 which is keeping the TB and candida in check
what regulates cortisol production
CRH stimualtes ACTH release and cortisol production. chronic stress induces it
increase in Ph does what to Ca homeostasis
it increases the affinity for albumin which draws Ca out of the free pool causing hypocalcemia effects
what does active vitamin D do
increases absorption of Ca and Po4 and enhances bone mineralization
what regulates vitamin D
increased PTH, decreased Ca, decreased phosphate, increase the production of vitamin D.
Parathyroid hormone function
increased bone resorption of Ca nada phosphate, increased kidney resorption of Ca in DCT, decreased resorption of phos in PCT, increased activation of vitamin D in PCT
where does PTH increase Ca respiration in kidney
DCT
where does PTH decrease phosphate reabsortion in the kidney
PCT
where does PTH increase vitamin D production in the kidney
PCT
what does increased RANKL do
it is secreted by osteoblasts and osteocytes which then bind to receptor in the class which breakdown the bone
which cancers produce parathyroid like hormone
renal cell carcinoma and squamous cell cancer of the lung
what increases PTH secretion
decreases Ca, increased phosphate, decrease Mg.
what happens if there is severely low Mg
it decreases PTH
what eznyme activates vitamin D in the kidneys
1 alha hydroxylase
what causes decreased Mg
diarrhea, aminoglycosides, diuretics, alcohol abuse
what does calcitonin do
oppose PTH and is from the parafollicular cells so it decreases resorption of bone
what are the functions of T3
brain maturation, bone growth, beta adrenergic, basal metabolic rate
what does thyroid hormone do to the heart
it increased B1 stimulation so increased CO, SVR, HR, and contractility
what does thyroid horomone do the BMR
increased Na/K ATPase activity so increased O2 consumption and RR and body temperatuer
what metabolic functions does thyroid hormone increase
glycogenolysis,gluconeogenesis, lipolysis
what increases TBG
pregnancy, estrogen, OCP- increased total T4 so less active hromone
what decreases TBG
it is decreased hy hepatic failure, steroids
wat converts T4 to T3
5 deiodinase
what is the wolff chaikoff effect
it is excess iodine temporarily inhibits thyroid peroxidase and decreases iodine organification and decreases T3 and T4 overall
What does thyroid peroxidase do
it oxidizes and organifies iodide as well as ccoupling MIT and DIT to form T3 and T4.
what does propylthiouracil do
it inhibits thyroid peroxidase and 5 diodinase
what does methimazole do
inhibits thyorid peroxidase only
cAMP pathway is which hormones
FSH, LH, ACTH, TSH, hCG, ADH, MSH, PTH, calcitonin, GHRH, glucagon
cGMP pathway is which hormones
BNP, ANP, EDGF (NO)
IP3 pathway is which hormones
GnRH, oxytocin, ADH, TRH, histamine, angiotensin II, gastrin
intracellular receptor pathway is which hormones
progesterone, estrogen, testosterone, cortisol, aldosterone, t3,t4, vitamin D
tyrosine kinase pathway pathway is which hormones
insulin, IGF, FGF, PDGF, EGF
JAK-STAT pathway
prolactin, IL2, IL6, IFN, GH, G-CSF, eryhtropoetin, thrombopoetin
what happens with increased sex binding globulin
gynecomastia from decreased free testosterone
what happens with decreased sex binding globlin in females
it raises free T and leads to hirsuitism
what increases sex binding hormone in females
pregnancy and OCP
what are sings of adrenal insufficiency
fatigue, weakness, hypotension, muscle aches, weight loss, GI disturbance, sugar and salt craving
primary adrenal insufficiency- what are the signs
hypertension from hyponatremic volume contraction, metabolic acidosis, increased potassium, and mucosal hyper pigmentation from the excess ACTH creating increased MSH.
what is the cause of acute primary adrenal insufficiency
sudden onset due to massive hemorrhage. Leads to massive shock and adrenal crisis- can be from waterhouse freinderichson with shock and DIC
chronic primary adrenal insufficiency
Addison disease- adrenal atrophy or destruction by autoimmune disease- can be destroyed by TB
secondary adrenal insufficiency
seen with decreased ACTH production. NO hyperkalemia or mucosal pigmentation- still get hypotension.
tertiary adrenal insufficiency
seen with withdrawal of long term steroids
hyperaldosteronism
increased secretion of aldosterone from adrenal gland leading to HTN, decreased or normal K and metabolic alkalosis but not edema
primary hyperaldosteronism
adrenal adenoma or conn or can be hyperplasia- get increased aldosterone and low renin
secondary hyperaldosteronism
see in patients with renovascular hypertension or JG cell tumor with increased aldosterone and renin, so there is no shut off of renin with aldosterone
neuroblastoma
adrenal medulla tumor of a child under 4 from neural crest cells can be along the sympathetic chain. It is a firm irregular mass that can cross the midline- causes dancing eyes and dancing feet
what is the different presentation between neuroblastoma and Wilms tumor
Wilms tumor is smooth and unilateral and neuroblastoma is firm, irregular and can cross the midline
what do you seen on labs for neuroblastoma
increased HVA and VMA and Homer wright rosettes with NSE and bombazine positive
what is the oncogene mutation in neuroblastoma
n-myc
pheochromocytoma
tumor of adrenal medullary chromatin cells which are from the neural crest
what mutations are pheochromocytoma associated with
NF1, VHL, RET,
what is the rule of 10s
10% are : malignant, bilateral, extra-adrenal, calcify, kids
what are the symptoms of pheochromocytoma
secrete NE and pi which epidoside hypertension, increased BP, headache, perspiration, palpitation, pallor
treatment for pheochromocytoma
use irreversible alpha antagonists like phenoxybenzamine followed by beta blocker
what should you not give first to treat pheochromocytoma
do not give beta blocker first it can create hypertensive crisis
hypothyrodism vs hypertthyroidism myopatyh
increased CK in hypothyroidism
what causes a smooth goiter
graves, hashi, iodine def, TSH adenoma
what causes a nodular goiter
toxic multinodular goiter, thyroid adenoma, thyroid cancer, cyst
hypoparathyroidism cause
due to accidental excision of parathyroid glands, autoimmune destruction, or Digeorge, tetany, hypocalcemia, hyperphosphatemia
Pseudomhypoparathroidism type 1A
unresponsiveness of kidney to PTH leading to decreased Ca with high PTH. can also see short 4/5 metacarpals, short stature. autsomal dominant with defect in Gs alpha subunit causing end organ damage resistance to PTH due to maternal imprinting
pseudopseudohypoparathyroidism
albright osteodystrophy but without end organ PTH resistance. Just from paternal Gs defect in alpha subunit.
familial hypocalciuric hypercalcemia
defective Ca sensing receptor in the kidneys and parathrougids so really high Ca levels cause the decrease in PTH so see high PTH to normal PTH with Increased CA- excessive renal repute of Ca
primary hyperparathrouid
usually due to adenoma or hyperplasia- hypercalcemina and uric- decreased phosphate. increased PTH- weakness, constipation, kidney stones, pancreatitis, depression can get bone lesions and peptic ulcers
secondary hyperparathyroidism
decreased Ca absorption and or increased phosphate from CKD and this leads to hypocalcemia, hyperphosphatemia in chronic renal failure.
tertiary hyperparathyroidism
hyperparathyroidism from chronic renal disease s increased Ca and PTH
osteitis fibrosa cystica
cystic bone lesions from osteoclasts and hemosiderin. hits the cortical bone, subperiodsteal thinning, subperiosteal in the hands and salt and pepper head
pituitary adenoma most common and how to treat
prolactinoma from the lactotrophs- use bromocrpitine
mass effect of pituitary
bitemporal hemianopia, hypopituitarism, headache
Nelson syndrome
elargement of an ACTH adenoma after the removal of adrenals and it removes the feedback so it gets bugger- get hyperpigm, headache, and bitemporal heminanopia
acromegaly
excess GH in adults- glucose tolerance
what is at increased cancer risk in acromegaly
colon polyps and cancer
what is the cause of death in gigantism
heart failure
what do you see with acromegaly labs
increased IGF1, failure to suppress serum Gh following oral glucose test
Laron syndrome- dwarf
decreased response to growth hormone because f lack of receptors- see increased GH and decreased IGF-1
diabetes insipidis Central
pituitary tumor, autoimmune, trauma, surgery, ischemic encephalopathy, synthesized in paraventricular and supraoptic nuceli- decreased ADH< but does respond to desmopressin
diabetes insipidis nephrogenic
hereditary ADH receptor mutation, can be second degree to hypercalcemia, hypokalemia, lithium, demeclocycline. Normal or increased ADH. cannot change in osmolality with administration of desmopressin.
treatment of nephrogenic DI
HCTZ, indomethacin, amiloride, hydration, avoid the offending agent
where does the lithium effect the nephrogenic DI
it hits the CT and it is normally excreted at PCT
what happens if the defect is in the hypothalamus
it is then permanent
SIADH- what are the characteristics
excessive free water retention, euvolemic hyponatremia with continuous urinary NA excretion, urinary osmolality>serum osmolality
SIADH physiological effects
decreased aldosterone, and increased ANP and BNP. There is increased NA secretion, normalization of extracellular fluid volume. euvolemic hyponatremia. Very low serum Na. This leads to cerebral edema, seizures. Correct to prevent demyelination syndrome
what can happen if there is rapid correction of hyponatreima
central pontine myelinolysis
what are the causes of SIADH
ectopic ADH (small cell lung cancer), CNS disorder or head trauma, pulmonary disease, drugs like cyclophosphamide.
Sheehan syndrome
ischemic infarcto f the pituitary following postpartum bleeding. Pregnancy induces pituitary growth, which then increases sociability to hypo perfusion. Usually presents with failure to lactate, absent menstruation, and cold intolerance
empy sella syndrome
atrophy or compression of pituitary which lies in the sella truck often idiopathic common in obese women
pituitary apoplexy
sudden hemorrhage into the pituitary gland often in the presence of an existing pit adenoma, usually presents with sudden onset severe headache, visual impairment,bitemporal hemianopsia, diplopia due to CN III palsy, feature of hypo pit can get cardiac collapse due to ACTCH and adrenocortical insufficiency
diabetes mellitus symptoms
polydipsia, polyuria, polyphagia, weight loss.
chronic complications of Dm- non enzymatic glycosilation
- nonezymatic glycosilation- small vessel disease- retinopathy, hemorrhage exudates, micro aneurysms, vessel proliferation, glaucoma, neuropathy, nephropathy and Kimmelsteil wilson nodules. progressive proteinuria, arterioloscrlosis, and hypertension
- large vessel issues of DM_ atheroscelorisis, CAD, peripheral vascular disease, gangrene, limb loss, cerebrowvascualr disease- MI is most common cause of death
what can be used to protect the kidneys from DM after microalbuminemia is started
use the ACE inhibitors
what is the osmotic damage from DM
sorbitol accumulation in organs with aldolose reductase and decrease or absent sorbitol dehydrogenase. Neuropathy, stocking glove, and autonomic degeneration, cataracts
glucagonoma
tumor of pancreatic alpha cells- overproduction of glucagon. Presents with dermatitis (narcoleptic migratory erythema), diabetes with hyperglycemia, DVT, declining weight, depression
treatment for glucagonoma
octreotide, and surgery
insulinoma
tumor of pancreatic beta cells, overproduction of insulin- hypoglycemia- may see whipple triad- hypoglycemia, lethargy, syncope, diplopia, resolution after normalization of glucose- decreased blood glucose and increased C peptide. some are associated with MEN 1
somatistatinoma
tumor of pancreatic delta cells,overproduction of somatistatin, decrease secretion of secretin, cholecystokinin, glucagon, insulin, gastrin- may present with diabetes, glucose intolerance, steatorrhea, gallstones.
treatment of somatistatinoma
somatistain analogs- octreotide and surgery
carcinoid syndrome
neuroendocrine tumor of rosettes, metastatic small bowel timers which secrete high levels of serotonin. not seen if the tumor is in the GI tract only. See diarrhea, flushing, asthmatic wheezing, right sided valve disease, tricuspid regurgitation, pulmonic stenosis, increased 5HIAA in the urine. Niacin deficiency and pellagra
treatment for carcinoid syndrome
surgical resection, somatistatin analog
rule of 1/3 with carcinoid syndrome
1/3 met, 1/3 have second malignancy, 1/3 are multiple- most common malignancy of the small intestine
pancreatic endocrine tumor, pituitary tumors, parathyroid adenoma- condition and mutation
MEN 1- mutation in menin and tumor suppressor gene on chromosome 11
parathyroid hyerplasia, medullary thyroid carcinoma, pheochromocytoma- condition and mutation
MEN 2A- ret mutation codes for receptor tyrosine kinase in cells of neural crest origin
medullary thyroid cancer, pheochromocytoma, mucosal neuromas, marfanoid- condition and mutation
MEN 2B- ret mutation
what develops if the lateral folds fail to close
omphalocele or gastroschisis
what develops if the caudal folds fail to close
bladder extrophy
what week foes the gut herniate through the umbilical ring
6
what week does the gut return and what does it rotate aroudn
it rotates around the SMA and its 10 weeks
extrusion of abdominal contents through abdominal folds- uncovered bowel
gastroschisis
persistence of herniation of abdominal contents into umbilical cord sealed by peritoneum
omphalocele
what is the most common type of TE
esophageal atresia with distal fistula
what are the symptoms of TE
drool, choke, on vomit with first feeding, air in the stomach on the stomach CX and cyanosis from laryngospasm and failure of NG tube to hit stomach
duodenal atresia
gailure to recanalize and dilation of stomach and proximal duodenum- associated with downs
what do intestinal atresias present with
bilious vomiting, and abdominal distention within the first 1-2 days of life
jejunal and ileal atresia
disruption of the mesenteric vessels leading to ischemic necroses and segmental reposition with bowel disontinuity- apple peal
olive mass, projective vomiting- what is it, patients typical, and what does it lead to with electrolytes
hypertrophic pyloric stensosis- it is first born males at 2-6 weeks old. It can be from macrolide exposure. It is hypokalemic, hypochloremic metabolic alkalosis from the vomiting
what forms the ventral bud of the pancreas
uncinate and pancreatic duct
what forms the dorsal bud of the pancreas
it is the body, till, isthmus, and accessory pancreatic duct
what does the annular pancreas form from and what does it strangulate
it encircles the second part of the duodenum, and it causes non-bilious vomiting- ventral buds encricle
what is pancreas divisum
it is where the dorsal and ventral buds final to fuse and they are usually asymptomatic or might have chronic pancreatitis
what is the embryonic origin of the pancreas and spleen
pancreas- endoderm
spleen- mesoderm
what are the retroperitoneal structures
adrenals, IVC, arota, duodenum (2-4), pancreas, ureter, colon, kidneys, esophagus,rectum
what part of the pancreas, colon, and duodenum are in the retroperitonem
pancreas- all but tail
colon- ascending and descending
duodenum- 2-4
how can blood get in the retroperitoneum during a cardiac procedure
it can be from the common femoral vein
where is a filter placed to prevent DVT from hitting the lungs in people who can’t take anticoagulants
in the IVC
on a transesophageal echo what is on the anterior and was is posterio
anterior- left atrium
posterior- descending aorta
if blaming the hepatoduodenal ligament does not stop bleeding where is the issue
IVC or hepatic vein
what is in the portal triad and what ligament is it associated with
proper hepatic artery, portal vein, common bile duct
what position of the gut wall has the meissner plexus and what has the myenteric plexus
meissener plexus- submucosa
myenteric plexus- muscularis externa
what is the difference between ulcers and erosions
ulcers erode into the submucosa and muscle layers, and erosions are mucosa only
where are the brunner glands and what are their purpose
they secrete bicarb and they are in the duodenum
where are the peyers pathcs
ileum
where are the largest number of goblet cells in the small intestine
ileum
what branches are at T12, L1, L2, L3, L4, L5
t12- celiac
L1-L2- renal gonadal, and SMA
L3- IMA
L4 bifurcation of the aorta
intermittant intestinal obstruction with postprandial pain what is compressed and what is compressing it
SMA is compressing the 3rd segment of the duodenum- this is the transverse part of the duodenum
esophageal anastomosis- clinical signs and what is the shunt
esophageal varices- left gastric to the azygous vein
umbilicus- clinical signs and what is the shunt
caput medusa, and paraumbilical to small epigastric veins of the anterior abdominal wall
rectum- clinical signs and what is the shunt
anorectal varices- superior rectal to middle and inferior rectal
when are these varices usually seen
portal HTN
treatment for varices
transjugular intrahepatic portosystemic shut between the portal vein and hepatic vein relieves the portal HTN by shunting the blood to the systemic circulation, bypassing the liver
what supplies about the pectinate line
superior rectal artery from the IMA- it drains to the portal ciruclation
what are the symptoms of internal hemorids
bright red blood with no pain
what is the lymph drainage about the pectinate line
it is to the internal iliac lymph nodes
what is the arterial suppliy and venous drainage below the pectinate line
it is inferior rectal artery off the internal pudendal artery and the venous drainage is to the IVC
what does the pudendal nerve supplie
perinemum and external gentialia with touch, temperature and pain.
what are the symptoms of external hemorids
painful from pudendal nerve and can blled
what is the lymph drainage of below the pectinate line
superficial inguinal nerves
anal fissure
pectinate line below, pain while pooping, blood, posterior because of poor perfusion from low fiber and constipation
what are kipper cells
specialized macrophages of the liver that line the sinusids
what do hepatic stellate cells store
vitamin A and can produce extracellular matrix
zone 1 liver - where is it, what affects it
periportal so near blood supply and it is affected by viral hepatitis, and ingested toxins like coke
zone2 liver- - where is it, what affects it
intermediate zone is hit by yellow fever
zone 3 liver- - where is it, what affects it
it is the pericentral centrilobular zone near the drain point- it is affects by ischemia, it houses the cytochrome p450 system and it is sensitive to metabolic toxins and it is the site of alcoholic hepatitis
where is the P45 site
zone 3
what is the flow of bile and blood through the zones
blood- 1-3
bile- 3-1
where would be the gall stone if it is causing cholangitis and pancreatitis
it is in the ampulla of vater
what can tumors in the head of the pancreas obstruct
common bile duct leading to painless jaundice
from lateral to medial what is the organization of the vessels of the femoral region
nerve, artery, vein, lymphatics (NAVeL)
what is in the femoral triangle
femoral nerve, artery, vein
what is in the femoral sheath
femoral nerve and artery and canal with deep inguinal LB but NOT the nerve
what side is the congenital diaphragmatic hernia on and what is it from
congential defect of pleuoperitoneal membrane occurs on the left side due to relative protects of the right side by the liver-
what is a hiatal hernia
it is where the stomach herniates through the esophageal hiatus
sliding hiatal hernia
LES moves up and there is an hourglass stomach
what is a paraesophageal hernia
gastroesophageal junction is usually normal and the funds protrudes into the thorax
indirect inguinal hernia- typical patients, where it dos and what is the origin of it
failure of the processes vaginalis so it can have a hydrocele as well. It enters at the external inguinal ring and internal ring and it slides into the scrotum and it is lateral to the inferior epigastric vessels. It is covered in all three layers of spermatic fascia
direct inguinal hernia
protrudes through the inguinal triangle and bulges through the abdominal wall medial to the inferior velds. It goes through the superficial ring and it is covered by external spermatic fascia
femoral hernia
protrudes below the inguinal ligament through the femoral canal below and lateral to the pubic tubercle. It is medial to the femoral vein and lateral to pubic tubercle it is inferior to the inguinal ligament- it is more likely to present with incarceration or strangulation
what forms the Hesselbach triangle
medial is lateral rectus
top- inferior epigastric vessels
lateral- inguinal ligament
gastrin is from, action, regulation
G cels of the antrum of the stomach and duodenum, and it increased gastric H secretion and increases growth of the gastric mucosa, and increases the gastric motility, it is increased by stomach distention/alkalinization, amino acids, vagal stimulation and decreased by PH<1.5
what increases gastrin
chronic PPI, chronic atrophic gastritis, ZE syndrome
somatostatin is from, action, regulation
D cells in the pancreatic islets and GI mucosa- it decreases gastric acid and pepsinogen secretion, it decreases pancreas and small intestine fluid secretion, decreases gallbladder contraction, decreases insulin and glucagon release- it increases with increased acid and decreases by vagal stimualtion
what is octreotide used for and what does it mimic
octreotide is a somatistatin analog that is used to treat acromegaly, carcinoid syndrome, and vatical bleeding.
somatistatin overall does what
decreases secretion of lots of hormones
cholecystokinin is from, action, regulation
I cells in the duodenum and jejunum- it increases pancreatic secretion, increased gall bladder contraction, decreased gastric emptying, increased sphincter of ODdi relaxation- increased by fatty acid amino acids-
CCK does what to pancreatic secretions
it boosts them and acts on neural muscarinic pathways to cause this
secretin is from, action, regulation
it is from S cells. It is kicked off by increased H and bicarb from the pancreas. It increases the pancreatic secretion of bicarb and decreases the gastric acid secretion and increases the bile sectarian. it is regulated by increased acid and fatty acids in the duodenum
why do you want bicarb secreted from S cells of the duodenum in the face of acid
it is from neutralizing the acid to allow the pancreatic enzymes to function
glucose- dependent insulinotropic peptide is from, action, regulation
it is from the K cells and it decreases gastric H secretion and increases insulin release in response to fatty acids, glucose and amino acids in the lumen of the duodenum It is also known as GIP
what hormone causes increased insulin secretion orally but does not work if glucose is through an IV
GIP stimulates extra insulin secretion so if glucose is through the stomach rather than the IV
motilin is from, action, regulation
motilin is from the small intestine and produces migrating motor complexes it increases in fasting state.
what are motion receptor agonists used for and what is an example
erythromycin is a motilin antagonist which stimulates peristalsis
vasoactive intestinal peptide is from, action, regulation
it is from ons ganglia in the sphincters, gallbladder, and small intestine- increased intestinal water and electrolyte secretion and increased relazation of intestinal smooth muscle and sphincters- increased by distention and vagal simulation decreased by SNS
VIPoma
non alpha and non beta cell islet tumor of the pancreas that causes watery diarrhea, hypokalemia, and achlorhydria (decreased gastric acid)
Nitric oxide is from, action, regulation (GI)
increased smooth muscle relaxation and LES- loss of NO secretion is implicated in the increased tone in achalasia
what does NO relate to achalasia
it is decreased which means the esophagus cannot relax
ghrelin is from, action, regulation
it is from the stomach and it increases appetite and it is increased in the fasting state and decreased by food. Increased in Prader Willi and decreased after gastric bypass
intrinsic factor is from, action, regulation
it is from the partietal cells and it creates the binding iwith B12 and it makes it ready for uptake in there terminal lileum
gastric acid is from, action, regulation
parietal cells of the stomach it decreases the ph- it is increased by histamine, each, gastrin and decreased by somatostatin, GIP, prostaglandin, and secretin
what increased gastric acid
ACH, gastrin and histamine
pepsin is from, action, regulation
chief cells of the stomach, protein digestion increased by increased vagal stimulation and local acid
what is the inactive source of pepsin
it is pepsinogen until its in the presence of H
bicarbonate is from, action, regulation
from mucosalcells and brunner glands to neutralize acid and it increased through pancratic and biliary secretion with secretin
amylase- what does is digest and anything special
it digests starch and is secreted in an active form
lipases- what does is digest and anything special
fat difestion
proteases- what does is digest and anything special
protein difestin inclues trypsin, chymotrypsin, elastase, and carboxypeptidases
trypsinogen- what does is digest and anything special
it is converted to active enzyme trypsin to activation of other proenzymes and cleaving of additional trypsinogen molecules into active trypsin. Converted to trypsin by enterokinase/enteropeptidase at bruch order
what happens if there is a deficiency of enteropeptidase
no tyrpsin so protein and fat malaspption, failure to thrive and edema
carbohydrate absorption
only monosaccharides are absorbed by enterocytes. Glucose and galactose are through SGLT1.
what is fructose taken up by
GLUT2
what takes up glucose and galactose in the intestine
SGLT1
what is the rate limiting step of carbohydrote digestion at the brush border
oligosaccharidase
what is the DXylose test
distinguishes GI mucosal damage from malabsoprtion
what is D xylose
it is still active without pancreatic enzymes and can decrease overgrowth of bacteria
where is iron absorbed
in duodenum
where is folate absorbed
small bowel
where is B12 absorbed
terminal ileum along with bile salts and requires intrinsic factor
what are peers patches, where are they, what do they have
unencapsulated lymphoid tissue in the lamina propr. and submusoca of the ileum contain specialized M cells that sample and present immune cells. Be cell stimulated in germinal centers of the eye patches differentiate into IgA secreting plasma cells which ultimately reside in the lamina propr.. IgA receives protective secretory comporntt to travell across the gut
what is the rate limiting step of bile acid synthesis
it is cholesterol 7 alpha hydroxylate
what are the functions of bile
digestion absorption of lipids and gat soluble vitamins, cholesterol excretion, and antimicrobial via membrane disruption
what is bilirubin conjugate with to make it direct billirubin
glucoronate
which bilirubin is soluble in water
conjugated
pleomorphic adenoma
benign mixed tumor. It is the most common it is chonromyxoid storm and epithelium and recurs if not complete exccises
mucoepidermoid carcinoma
malignant salvart tumor with squamous and mucous components
warthin tumor
papillary cystademona lymphomatosum- benign cystic tumor with germinal centers
which salivary glands are more malignant
submandibular or sublingual
which nerve is usually involved in the salivary gland tumors
VII
which nerve is usually involved in the salivary gland tumors
VII
achalasia
failure of relaxation of LES due to loss of myenteric plexus. High LES resting pressure and uncoordinated peristalsis. Progressive dysphagia.
what can cause achalisia secondarily
Chugs disease or mass effect
boerhaave syndrome
transmural usually distal esophageal rupture with pneumomediatum- due violent retching surgical emergency
eosinophilic esophagitis
infiltration of eosinophils into the esophagus often in atopic patients. food allergens- dysphagia, food impugn. rings and linear furrows often seen on endoscopy
what causes strictures in the esophagus
associated with caustic and acid reflux
esophageal varices
dilated submucosal veins in the lower 1/3 if esophagi second degree to portal HTN.
esophagitis with linear ulcers
CMV
esophagitis with punched out lesions
HSV
GERD
heartburn, regurgitation, dysphagia. Chronic cough and hoaarsenss
Mallory Weiss syndrome
mucosal lacerations that are linear- gastropeal junction from sever committing with the hematemisis- due to abdominal pressure
Plummer Vinson syndrom
dysphagia, iron deficiency, anemia, esophageal webs- glossitis
scelerodermal esophageal dysmotility
esophageal smooth muscle atrophy because of decreased LES pressure and dysmotility and acid reflux and dysphagia, stricture, barrett esophagus, ad aspiration part of CREST
barrett esophagus
specialized intestinal metaplasia- replacement of nonkeratozined stratified sqamous epithelium with intestinal epithelium. with goblet cells and in distal esophagus. Due to chronic reflux esophagitis GERD. Associated with increased risk of esophageal adenocracinoma
squamous cell carincoma esophagus
upper 2/3 and alcohol, hot liquids, caustic strictures, smoking, achalasia- more worldwide
adenocarcinoma esophagus
lower 1/3 and chronic GERD, Barrett esophagus, obesity, smoking, achalasia- america
acute gastritis- what causes it
erosions in the mucosa from NSAIDs- PGE2 decrease, decreased gastric mucosa protection
burns-Curling ulcer- hypovolemia- mucosal ischemia
brian injury- increased vagal stimulation- ACH increase, increase H production
chronic gastritis- what causes it
mucosal inflammation often leading to atrophy hypochloridia, hypergatrinemia and intestinal metaplasia and increased risk of gastric cancer
h pylori
most common to increase risk of peptic ulcer disease, MALT lymphoma
autoimmune chronic gastritis
autoantibodies to parietal cells and intrinsic factor and increase risk of pernicious anemia- affects body/fundus of stomach
menetrier disease
gastric hyperplasia of mucosa- hypertrophied rug, excess mucus production with resultant protein loss and parietal cell atrophy with decreased acid production- precancerous
gastric cancer intestinal kind
associated with h pylori, dietary nitrosamines, tobacco, achlorhydria, chronic gastritis. commonly on the lesser curvature looks like ulcer with raised margins
gastric cancer diffuse kind
not associated with hpylori- signet ring cells- mucin filled cells and stomach wall grossly thickened and leathery stomach
virchow node
icolvement of the left supraclaviculaar node by mets from stomach
Krukenberg tumor
bilateral metases to ovaries. Abundant mucin-secreting, signet ring cells
sister mary joseph nodule
subcutaneous periumbilical metatsis
gastric ulcer
usually h pylori, decreased mucosal protection against gastric acid. NSAIDs can be increased risk carcinoma. greater pain with meals and weight loss
duodenal ulcer
decreases with meals and weight gain. mostly h pylori. Decreased mucosal protection or increased gastric acid secretion. ZE syndrome, generally benign and hypertrophy Brunner. posterior wall rupture leads to gastroduodenal artery rupture
what is the blood vessel that can be eroded with an duodenal ulcer
gastroduodenal artery
if there is an ulcer on the lesser curve
bleeding from left gastric artery
what referred pain with duodenal ulcer
duodenal perforation with air under the diaphragm
systemic mastocytosis
abnormal mast cell proliferation and increased histamine release. Hyper secretion of gastric acid by parietal cells in the stomach as well as hypotension, flushing, puritis
lactose intolerance
lactase deficiency- normal appearing villi, when second degree to injury at tips of villi, osmotic diarrhea with decreased stool pH. viral enteritis can cause it. Lactose hydrogen breath: positive for lactose malabsorption if post lactose breath hydrogen value rises>20ppm compared with baseline
pancreatic insufficiency
due to chronic pancreatitis, cystic fibrosis, obstructing cancer- causes malabsorption of fat and fat soluble vitamines- ADEK as well as B12- decreased duodenal pH and decal elastase
old man with weight loss, diarrhea, abdominal pain, and increased excretion of fat and muscle
pancreatic insufficiency
tropical sprue
celiac sprue, affects bowel but responds to antibiotics but seen in residents of or recent visitors to tropics- decreased mucosal absorption affecting duodenum and jejnum but can involve ileum with time. associated with megaloblastic anemia due to folate deficiency and B12 deficiency
whipple disease
infection with trophynema while +PAS, foamy macrophages, cardiac syndromes, arthralgia, neurologic symptoms.
middle aged men with long term malabsorption and cardiac, psych and arthritis
whipple disease
what causes appendicitis
due to obstruction by facecloth or lymphid hyperplasia in children,
