Pathoma- endocrine zhester
Terms in this set (314)
Adenoma of Pituitary is benign or malignant?
benign and it can produce hormones or it may not
What happens if the Adenoma is NONFUNCTIONAL?
then it has a MASS EFFECT- where it starts compressing different regions of the brain
what happens if the Pit adenoma becomes BIG and it starts compressing the optic chiasm?
bitempotal hemianopsia. b/c the pituitary sits next to the sellica turcica and right next to it is the optic chiasm
which part of the vision would be compromised with pituitary adenoma compressing the optic chaism? peripheral or near?
both eyes would lose their peripheral visions- the 1/4 ends of the nerves which come and cross over at the optic chiasm.
what happens to the near sided nerves which are 3 and 2?
they never go through the optic chiasm- they are most laterally?
what is hypopituitary
you have an an external tumor and it starts compressing the normal pituitary- and you will see loss of the function of the normal pituitary
what are the three features that can present with NONFUNCTIONAL TUMORS?
1. bitemporal hemianopsia
BITcHH (nonfunctiona) BITemp, (c), Hypopit, Headachr
what is the difference between functional and nonfunctional pituitary adenomas?
funcitonal produces hormones and the other one does NOT.
what is the most COMMON functional tumor of the pituitary?
what effect does prolactin have on the BREAST?
milk Production (P-P)- so you will get galactorrhea
what role does prolactin have on the reproductive cycle?
it INHIBITS GnRH synthesis. and If you have TOO MUCH prolactin then you will keep inhibiting gnRH synthesis and subsequently LH/FSH release leading to AMENORRHEA
what are the signs and symptoms associated with proactinoma in males? femaleS?
males- decreased libido and headache
why don't men have galactorrhea with prolactinoma?
because Terminal duct --> lobular unit formation which are subunits of the breast are NOT formed in males- so they will not have any milk production which prolactin induces in the lobular units
what is the treatment for prolactinomas?
dopamine agonist- because that INHIBITS prolactin secretion or surgery
what is an example of a dopamine agonist?
Bro- uses drugs to dope
what are the symptoms associated with proactinoma in males vs females?
males- dec libido and headache (headache MD libido)
females- galactorrhea and amenohrrhea FAG
what do children have gigantism with growth hormone adenoma?
because children do not have their EPIPHYSEAL PLATE FUSION- so they will get continual growth and that will result in GIGANTISM.
why is the symptom associated with growth hormone adenoma in adults?
they get acromegaly- they would induce the growth of areas OUTSIDE the epiphyseal plate fusion- such as heart, lungs, tongue, bones, hands, feet and jaw.
what is the most common cause of death in acromegaly?
what role does GH have on glucose?
it DECREASES glucose uptake
what happens to the glucose levels in growth hormone adenoma?
GH- (-) inhibits glucose uptake- so then you will have secondary diabetes
what other hormone does GH induce which plays a role in insulin levels?
GH goes to the LIVER and induces the release of insulin like growth factor 1
elevated GH causes IGF-1 increase and that mediates the glucose uptake in tissues inducing growth.
how do we differentiate between GH adenoma vs. GH over secretion?
oral glucose would suppress GH secretion, but it would have NO EFFECT on the GH adenoma
what is the treatment for GH adenoma?
octreotide- it is a somatostatin analog and it will decrease the release of the GHRH from the hypothalamus.
what are 3 methods to treat GH adenoma?
1. to decrease the release of the hormone (octreotide)
2. to inhibit the the hormone to act on the site of activity (GH antagonist)
what are some other adenomas associated with the pituitary?
TSH/LH/FSH adenomas ARE RARE
when do you start seeing symptoms associated with hypopituitarism?
when you have LOST 75% of the parenchyma
what are the causes of hypopituitarism in adults?
Pituitary adenoma. (because the pituitary will GROW and it will lead to the LOSS of the pituitary)
what is apoplexy?
bleeding into the adenoma- and that will cause INCREASE in the growth of the adenoma- and that will start compressing the surrounding tissues.
where does craniopharyngioma come from?
sellica turicica. and that can start compressing the normal pituitary tissue. associated with CHILDREN
when does sheehan syndrome occur?
what happens to the pituitary in the sheehan syndrome?
it doubles in size because during pregnancy there is HIGH demand of hormones. However, through the pituitary INCREASES in size, it doesn't mean that the blood supply is KEPT up. and has signs to undergo INFARCTION
what happens to a woman with sheehan syndrome and gives birth?
during birth it LOSES a lot of BLOOD- and it is susceptible to INFARCTION.
what are the symptoms associated with sheehan syndrome?
poor lactation and loss of pubic hair
why do you get loss of pubic hair in sheehan syndrome?
because you have LOSS OF LH - and that is responsible for production of the androgens and thats responsible for the growth of pubic hair.
What is empty Sella syndrome?
thats when the pituitary is MISSING from the sellica turica
what is the cause of Empty Sella syndrome?
1. trauma- which causes the pituitary to be DAMAGED.
2. congenital DEFECT of the sella- in which you have arachnoid herniation into the sella compresses the pituitary
describe the anatomy of the sella diaphragm and how it is associated with arachnoid herniaiton causing empty sella syndrome?
sella diaphrgram is covered by the dura and then the arachnoid. And then pituitary is covered by the pia. If you have arachnoid herniation- then you will have compression of the pituitary and cause it to be destroyed
what are the hormones secreted by the post pituitary? are they made there? what are their function and the site of action?
ADH/Post (secreted), but made in the hypothalamus. And ADH role is to increase the UPTAKE of water from the CT and DCT. And Oxytocin functions to increase the UTERINE CONTRACTIONS and lactation response.
what does diabetes mean?
someone is urninatng TOO MUCH
what is diabetes INSIPIDUS?
thats when you have ADH deficiency- that means you are not UPTAKING enough water to match the osmolarity of the plasma and secreting all of it out.
where are the two regions where Central Diabetes Inspidus is produced?
hypothalamic (b/c thats where the ADH is produced) and Post Pit (thats where it is SECRETED FROM).
what is polyuria?
urinating too much due to LACK OF ADH
What is polydipsia?
you have too drink too much water due to a lot of secretion of ADH
why do you get hypernatremia associated with ADH def?
you are secreting WAY TOO MUCH water- that means you are concentrating the plasma. and leading to hypernatremia. and subsequently HIGH SERUM OSMOLARITY
how would the ADH def look like?
low serum osmolarity and low specific gravity
how do you make the diagnosis of ADH deficiency?
water deprivation test- because if you deprive water- then ADH would go up- to maintain the osmolarity within the serum and subsequently the osmaolity in the urine would GO UP (because your keeping the excess water). however ADH deficient patient would have not be able to increase the urine osmaility.
what is the treatment for Diabetes Inspidus (Pituitary- central-Cfor CNS)
Desmopressin (ADH analog)
what is Nephrogenic Diabetes Insipidus?
the receptor in the kidney are unresponsive to the ADH. (impaired RENAL response).
what are some of the causes of the diabetes Inspidus?
drugs such as LITHIUM AND democyclin and inherited mutations
how do you differentiate between Nephrogenic and Central Diabetes Insipidus?
the symptoms associated with neph/central are the same, however desmopressin is the only differentiating factor
CNS- responsive to DESMOPRESSIN
Nephrogenic- UNRESPONSIVE to desmopressin because even though you give ADH analog- it doesn't matter if the RECEPTORS are not working.
what is SIADH?
when you have TOO MUCH ADH SECRETION
what are the clinical features?
hyponatremia (you will keep holding up too much wateR)/low serum osmolality
why do you get mental status changes and seizures associated with SIADH?
swelling of the nerves and cerebral edema
what are the causes of SIADH?
1. pulm infection
2. Ectopic production
3. CNS trauma
what can cause ectopic production?
small cell carcinoma- which is associated with ectopic production of the ADH
what drug is associated with increase in ADH secretion?
what is the treatment for SIADH?
free water restriction
what is democyclocine?
that will inhibit the SIADH secretion
What is "anterior neck mass" a sign of?
thyroglossal duct cyst- the thyroid develops at the base of the toungue-and it travels along the thyroglossal duct to the anterior neck. And if it involutes- persist-it will make anterior neck mass.
what is lingual thyroid?
persistence of thyroid tissue at the base of the tongue. and it presents as a base of the tongue mass
what do you see in hyperthyroidism?
1. increase BMR
2. increases sympathetic nervous system activity
how does Thyroid increase the BMR?
1. it activates Na/K ATPase activity
how does thyroid increase the sympathetic activity?
by increasing the B1 adrenergic activity
what are the clinical features associated with hyperthyroidism?
1. weight loss despite increased appetite
2. heat intolerance and sweating
3. tachycardia with increased CO
4. arrythmia (a fib) esp in elderly
5. Tremor, Anxiety, insomnia and heightened emotions
6. staring gaze with lid lag
7. diarrhea with malabsorption (the gut is moving faster)
9. bone resorption with hypercalcemia
10. decreased muscle mass with weakness
why does hyperthyroidism cause hypocholesterolemia/hyperglycemia?
thyroid causes gluconeogenesis and glycogenlysis
T/F Follicular Adenoma is surrounded by fibrous capsule?
Do follicular Adenoma secrete thyroid hormone?
False- they are usually nonfunctional
what is the distinguishing feature of follicular Adenoma?
it is surrounded by dense capsule. (however it still contains the follicles with colloid- but it contains a dense capsule which is clearly demarcating the tumor).
what are 4 types of carcinoma associated with thyroid?
Thyroid of FAM PAPs?
Thyroid- Follicular/Anaplastic/Medullary- Pap?
what is 80% type of the thyroid carcinoma?
what is the cause of papillary carcinoma?
ionizing radiation in childhood is a major risk factor esp in childhood when you are radiating the face for acne/ radiating the neck too- so papillary cardinoma
what is the key distinguishing feature of papillary carcinoma?
nuclear structures- in which there is WHITE CLEARING at the central of the nucleus. so you have orphan head nuclei- and there is presence of the nuclear groove (line within the nuclear groove)
what is psomma bodies?
you get different architecture associated with calcifications.
what is it called when you have IgG at the TSH receptor?
how is this autoimmune disease different from other?
other ones- would DESTRUCT THE RECEPTOR- which would lead to the reduction in the response,
Graves dx- is STIMULATION- INDUCTION of the TSH receptor
what happens if you have TSH receptor activated?
it leads to increased synthesis/release of TH
what is the most common cause of hyperthyroidism? when does it occur?
grave's- women childbearing age
what are the clinical features associated with grave's?
1. hyperthyroidism- TSH causes inc in thyroid production
2. diffuse goiter
3. exophthalmos and pretibial myxedema
why do you get diffuse goiter?
you get an Ab against the TSH receptor-then you get massive hyperplasia/massive hypertrophy of the gland diffusely. -- diffusely enlarged thyroid.
why do you get exopthalmos?
because you have TSH receptors in the eye- and Ab against it- will lead to the production of the GAG -- and the eye gets pushed forward.
why do you have pretibial myxedema
TSH also present in the shins-
edema refers not to the WATER, but to the GAG. AND IT IS myxoidy substance in which it is dull like appearance- or consistency towards the tissue.
it has HYPERPLASIA of the follicles- and it is VERY HUGE.
what is "scalloping of the colloid"?
it is a feature of the grave disease. Normally you have colloid filled up to the point that it is touching the epithelium. however, in hyper plastic colloid- there is colloid but it is NOT TOUCHING THE epithelium- and it has these white scalloping spaces in between.
what are the labs for graves?
since it is hyperthyroidism- which is depending on the number of T3/T4.
so it would be
INC IN TOTAL AND FREE T4
dec in TSH and hypocholesterolemia and increased serum glucose
why do you have low TSH
high amount of free T4 would lead to negative feedback inhibition and ultimately down regulation of the TSH
why would patients with grave's have hypocholesterolemia?
because it increases gluconeogenesis
why does it cause increase in serum glucose?
hyperglycemia- in which there is increased serum glucose
what is the treatment for grave's?
1. beta blockers- because thyroid increases the effects of the sympathetic system
what is the MOA of Thiomide?
it inhibits the production of the peroxidase
how is thyroglobulin madE? what is its precursor? and where is it secreted?
tyrosine--> thyroglobulin-->(which gets out into the Follicular lumen).
what is organification? where does it occur?
thats when the I2 from the follicles transported into the lumen which had I2 on them- it will lead to the I2 formation + thyroglobulin formation
so monoiodine + diiodine + thyroglobulin= T3
mono+diodo+ Thyroglob= T4
what does peroxidase do?
what enzyme does thiomide act on?
what is the purpose of Radioiodine ablation?
In grave's dx- the thyroid gland is excessively working- so you want to STOP IT. Since the thyroid uptakes the iodine from the external environment to undergo organification to make functional T3/T4. You would radio iodine it so then when it uptakes it it would have a radioactive analog attached to it which would be accessible for ablation
what is Thyroid storm?
surgery or childbirth- thats when you have elevated catecholamines and massive hormone excess (stress).
what are the symptoms associated with thyroid storm?
what is thyroid storm mediated by?
PTU, B blockers, and stress
what is the function of PTU?
it inhibits peroxidase- and organification/oxidation/coupling.
how does PTU dec the levels of T3?
T4 to T3 peripheral conversion and T3 is THE MORE ACTIVE FORM.
what is multi nodular goiter?
enlarged thyroid gland with multiple nodules. It is due to relative iodine deficiency. (b/c some foods can cause iodine def)
what is euthyroid?
it is NONTOXIC- that means it has no effect on other stuff
what is "toxic goiteR"?
thats when the regions become TSH independent- and it is producing EXCESS amount of Thyroid hormones independent on TSH stimulation
what is it called when you have HYPOthyroidism in infants/neonates?
what are the clinical features associated with hypothyroidism?
1. mental retardation
2. short stature with skeletal abnormalities
3. coarse facial features
4. enlarged toungue
5. umbilical hernia
why do you get mental retardation?
Thyroid hormone is necessary for the brain development
why do you get short stature in cretinism?
because thyroid hormone is necessary for the skeletal/bone development
what OTHER clinical features associated with cretinism?
coarse facial features
what are the causes of cretinism?
1. maternal hypothyroidism during EARLY PREGNANCY
2. thyroid agenesis
3. dyshormonogenetic goiter- in which you are DEFICIENT in peroxidase
4. iodine deficiency
what is the common enzyme deficient in dyshormonogenetic goiter?
what is it called when you hypothyroidism in adolescent/child or adult?
why do you have myxedema?
you have increase amount of GAG in soft tissues and skin.
why do you have deepening of the voice associated?
because you have increase amount of GAG and that leads to compression of the larynx and the enlarged tongue.
weight gain despite NORMAL WEIGHT GAIN, slowing of mental activity, muscle weakness, and cold intolerance with decreased sweating, bradycardia with dec CO, oligomenorrhea, hypercholesterolemia, constipation
what are the causes of myxedema?
1. iodine deficiency
2. hashimoto thyroiditis
4. surgical removal of radioblation
what is it called when you have AUTOIMMUNE destruction of the thyroid gland?
what disease is associated with HLA-DR5?
hashimoto- automimmune destruction of the thyroid gland
T/F patient with hypothyroidism has high amount of T4 initially
false, initially it presents as hyperthyroidism because when you have autoimmune destruction of the thyroid gland- then thyroid hormones they LEAK OUT OF THE TISSUES and there will be HIGH AMOUNT in the SERUM. and then it will normalize (euthyroid) and then it will come DOWN.
what are the diagnostic- TSH and T4 of hashimoto?
T4 low and high TSH
what are the markers that the thyroid has been DAMAGED?
anti-THYROGLOBULIN and anti-MICROSOMAL antibodies
what do you see in histo of the thyroid gland?
chronic inflammation + Germinal center + hurlel cells
what is a complication of the thyroidtism associated with GC? long standing hashimoto thyroiditis?
marginal cell lymphoma
B cell lymphoma.
GC--> Marginal cell lymphoma?
what are the hurthel cell change?
the cells that normally surround the follicles- they start turning PINK.
what is subacute (dequervain) granulomatous thyroiditis?
thats when you have it AFTER THE ACUTE process
what is the cause of the SGT?
If a patient has a "tender thyroid"?
subacute granulomatous thyroiditis
what presents with SGT?
1. presents as tender thyroid with TRANSIENT HYPERTHYROIDISM
2. self-limited, does NOT PROGRESS to HYPOTHYROIDISM
Reidel Fibrosing thyroiditis
"hard as wood"?
Reidel Fibrosing thyroiditis
what is Reidel fibrosing thyroiditis?
chronic inflammation with EXTENSIVE fibrosis of thyroid
T/F Reidel fibrosing Thyroiditis presents as HYPERthyroidism
presents as HYPOTHYROIDISM with "hard as wood", NON-TENDER thyroid gland
what does it do to surrounding structure?
fibrosis- it may extend to local structures (airway)
Thyroid lesion involving various structures surrounding it young female
Reidel Fibrosing thyroiditis
what about same condiiton- Thyroid lesion but OLDER?
Thyroid gland- with a DISTINCT solitary nodule.
Thyroid neoplasia are usually BENIGN or MALIGNANT?
what is the purpose of the 131 radioactive uptake studieS?
to differentiates various types of thyroid diseases
what diseases would you have INCREASED uptake in 131 radioactive uptake studies?
grave's dx or nodular goiter
what diseases would increase the uptake of Iodine?
graves dx or nodular goiter
what diseases DECREASES the uptake?
adenoma and carcinoma- that warrants FNA biopsy
follicular adenoma is distinct?
the presence of the capsule. Dense PINK CAPSULE.
what can you potentially get if you ionize radiation in childhood due to ACNE and it if it is IN THE FACE, it can go to the neck to?
what is distinct in histopath of papillary carcinoma?
papilllary finger-like projections-
nuclear features are what defines the papillary carcinoma-and thats when you have orphan-hide nuclei
what is the orphan hide nuclei?
there is white clearing in the nuclei
presence of the wideline or groove?
nuclear groove- sign of
what are psosmma bodies?
papillary architecture and the presence of the psomma bodies which is concentric calcifications-
layers of calcifications- and thats when you have LAYERING of the calcium and thats also known as PSOMMA BODIES-
what is the prognosis associated with papillary carcinoma? where does it usually spread?
cervical region- however, if ti spreads to the LYMPH NODES- then it still has EXCELLENT PROGNOSIS
what is follicular carcinoma?
malignant proliferation of the follicles.
what is follicular carcinoma?
Adenoma is confined to the capsule, however in follicular carcinoma there is invasion through the capsule.
tumor beyond capsule?
can you distinguish between Follicular carcinoma vs adenoma in FNA biopsy?
NO, because it is ONLY biopsy the follicular cells and you don't know what is going on in the CAPSULE.
gross/micorscoy of everything
how does follicular carcinoma spread?
spread through hematogenous
how is follicular carcinoma different from others?
normally, carcinoma is SPREADS through the LYMPH NODES. however, follicular CARCINOMA it spreads through the the BLOOD.
what are the four carcinomas that defy the principle that normally carcinomas are spread through the lymph nodoeS?
what are medullary carcinoma?
malignant proliferation of Parafollicular C cells.
what do parafollicular cells in the thyroid produce?
what is the purpose of the calcitonin
TONE DOWN the Calcium
so what would the patient with parafollicular tumor- medullary carcinoma have?
where does calcitonin deposit?
within the tumor as AMYLOID
what is the cause of medullary carcinoma causing?
malignant cells- in amyloid stroma
multiple endocrine neoplasia-
1. medullary carcinoma of the thyroid
1. medullary carcinoma of the thyroid
3. ganglioma of the oral mucosa
what mutation is associated with familial medullary carcinoma?
If there is RET mutation associated with familial predisposition to the prophylactic thyroridectomy?
then it is RET mutation
If an elderly patient comes in and has dysphagia and respiratory compromise?
If a young patient comes in and has dysphagia and respiratory compromise?
Reidel Fel Carcinoma
what is anaplastic carcinoma?
so it is an Undifferentiated malignant tumor of the thyroid. and it is usually seen in the ELDERLY. And it INVADES the local structures LEADING TO dysphagia or respiratory compromise.
what is the prognosis associated with ANAplastic carcinoma?
what is anapestic carcinoma?
highly malignant cells- resemble- undifferentiated carcinoma
what cells are unique to the Parathyroid gland?
what do the chief cells secrete?
What is the total level of Ca?
Ca bound to the proteins
Ca bound to phosphate
What kind of Ca does the chief cell regulate?
serum (free) ionized Calcium by the PTH
When is PTH secreted by the chief cells?
when the Calcium is LOW within the BLOOD.
what goes up when you have PTH secretion?
1. inc in bone osteoclast activity
2. inc in small bowel absorption of Ca and phosphate
3. inc in renal calcium reabsorption and
4. decrease in phosphate reabsorption
what does PTH do?
PTH--> activates the osteoblasts--> osteoclasts- and that resorbs bone- and releases calcium and phosphate into the serum
what effect does PTH have on the small bowel?
it increases small bowel absorption of Calcium and phosphate
what effect does PTH have on the renal?
and it increases the renal calcium reabsorption and decreases the phosphate reabsorption
what is primary hyperparathyroidism?
primary place - excess PTH due to the parathyroid
what is the most common cause of primary hyperparathyroidism?
what is primary hyperparathyroidism?
BENIGN, hypercalcemia and ASYMPTOMATIC
what are the consequences associated with increased PTH and hypercalcemia?
3. CNS disturbances
4. Constipation- peptic ulcer dx, acute pancreatitis
5. osteitis fibrosa cystica
what effect would parathyroid adenoma have on kidney?
neprholithiasis- in which you have KIDNEY stones- Calcium oxalate stones
what is nephrocalcinosis?
metastatic calcification- thats when you deposit Ca in the tubules of the KIDNEY. and that can lead to renal insufficiency and polyuria- aand that leads to hypercalcemia.
what happens to the CNS with Parathyroid adenoma?
Ca deposition in the CNS-- causes CNS disturbances and Seizures
what other symptoms?
what is the role of Ca on enzymes?
high amount of Calcium- and that is an enzyme ACTIVATOR- and that leads to increase in en
why do you get osteitis fibrosa cystica?
because you have high amount of Calcium and it is depositing in the BONE and it is causing osteitis fibrosa cystica- associated with hemorrhages
what do you see in nephrocalciunosis?
tubules- it contains Calcium- and it is being deposited in some of the tubules-
what are the lab findings associated with PTH?
1.high serum PTH
2. high serum calcium
3. low serum phosphate
4. increase in urinary cAMP
5. increase in alkaline phosphatase
Gs--> AC-> ATP-> CAMP-->
what is the difference between primary vs secondary hyperthyroidism?
primary- the actual source
secondary- something extrinsic
what is secondary hyperparathyroidism?
excess production of PTH due to disease process extrinsic to the parathyroid gland. And the common cause is CHRONIC RENAL FAILURE
what is the role of kidneys on phosphate?
decreases phosphate excretion
what effect would renal insufficiency have on the parathyroid gland?
renal insufficiency would prevent the phosphate EXCRETION. and retained Phosphate would combine with the "free calcium" making Calcium phosphate- And Chief cells which senses "low amount of FREE calcium" would be detected. And that would lead to INCREASE IN the PTH secretion- leading to ALL FOUR PARATHYROID GLANDS excited and that will lead to INCREASE in PTH which would lead to BONE RESORPTION
why do you have high amount of alkaline phosphatase associated with renal insufficiency?
because you have low amount of serum Calcium- and that leads to inc amount of PTH which would HIT THE BONE (inducing osteoblast activity) and that would lead to inc in ALKALINE PHOSPHATASE activity
what are the causes of hypoparathyroidism?
autoimmune damage, surgical excision, and DiGeorge syndrome
how does hypoparathyroidism present as?
2. muscle spasms (tetany)
3. low PTH and low Serum calcium
what is pseudohypoparathyroidism?
end-organ resistance to PTH. the receptors of PTH are NOT RESPONDING.
what is happening with pseudohypoparathyroidism?
hypocalcemia with increase in PTH levels
IF a patient has short stature and short 4th and 5th DIGITS?
what are islets of Langerhan cells?
units of the endocrine pancreas
what does each single islet consist of?
multiple cell type which produce ONE TYPE OF hormone
what cell secretes insulin?
what receptors are unregulated by the Insulin?
GLUT4- up regulation of it leads to increase uptake of the glucose in the peripheral tissues and muscles
what is the role of the alpha cells?
what is type 1DM?
insulin deficiency- metabolic disorder- HYPERGLYCEMIA
what is type1 DM associated with?
It is associated with HLA-DR3 and DR4
what is autoimmune destruction of the beta cells by the T lymphocytes?
thats when you have inflammation of the islets. and thats when you autoantibodies against the insulin
why do children with type 1DM have weight loss?
because they have no insulin to uptake into the peripheral tissues so weight loss
why do they have low muscle mass?
because they can't take it up in the muscle due to low levels of GLUT4 receptor up regulation due to lack of insulin- so the body is in energy deprivation form- and that will lead to low muscle mass. (a lot of glycogenlysis)
what is polyphagia?
they eat a lot
what is polyuria?
they have high glucose in the blood- high filtration by the kidney-thtas an osmotically active substance which will draw blood with it. and thats when you have polyuria with glucose in the blood with it.
what are the complications associated with DKA?
1. excessive serum ketoacids
2. often arises with stress
what happens in stress to lipoysis?
stress-->epinephrine--> glucoagon--> lipolysis--> inc in the free FA--> liver -->ketone bodies (beta butyric acid and acetoacetic acid)
why do you have hyperglycemia?
gluconeogenesis-/glycogenlysis associated an inc in the glucoagon as well
1. hyperglycmeia (>300 mg/dl)
2. anion gap metabolic acidosis
what is the role of Insulin on K?
insulin drives K INTO the cell. And so it will just stay outside.however, most of the EXCESSIVE K would be depleted and will be secreted out of the body.
DKA- anion gap metabolic acidosis-
what is kussmaul respirations?
high amount of CO2 blow off
what happens to the breath?
fruity smell- actone
what is the TREATMENT?
3. replacement of electrocytes
obesity--> will lead to DECREASE NUMBERS OF insulin receptors-
insulin is high in the beginning, but then there is DECREASED amount of insulin due to BETA CELL EXHAUSTION
the patient will present with polyuria/polydipdia/hyperglycemia
diabetes diagnosis?- what is the normal glucose level? fasting glucose? glucose tolerance test?
random glucose >200 mg/dL
fasting glucose > 126 mg/dlL
glucose tolerance test > 200 mg/dL two hours after glucose load
what happens if you have > 500 mg/dL of glucose?
then you have hypoerosimolar nonketotic coma
Are ketones present in hyperosmolar NON-ketotic coma?
no, ketones are ABSENT
what are the signs and symptoms associated with hyperOSMOLAR non-ketotic coma?
hypotension and coma
what happens in NEG of vascular BM of large/medium sized vessels?
what happens in NEG of small vessels?
what happens in NEG of hemoglobin?
thats what you detect for diabetes diagnosis of HbA1c
preferential involvement of the EFFERENT arteriole which would INCREASE IN THE PRESSURE in the glomerulus--> causing HYPERFILTRATION INJURY
HYPERFILTRATION INJURY- microalbuminuria
you will get sclerosing of the mesangium
arterial sclerosis of the AFFERENT arteriole- and that will lead to DIFFUSE SCLEROSIS lead to chronic renal failure
NEG of the HB- HbA1c-
what are some cells that have the ability to take up sugar WITHOUT insulin?
1. schwann cells
2. pericytes of retinal blood vessels
1. Schwann cells- takes up glucose readily- and that will lead to uptake of the glucose - aldose reductase--> sorbital. And thats why you get neuropathy
pericytes of retinal blood vessels- they can take up sugar in the blood vessels of retina-
endothelial cells on the BM on the vasculature- and the pericytes. sugar goes into the pericytes- causes osmotic damage-- and that will cause ANEURYSMS
high amount of glucose will go into the LENS--> aldose reductase
what is pancreatic endocrine tumors?
tumors of the islet cells- and they are a component of MEN1-
what is insulnoma?
episodic hypoglycemia with mental status changes that are relieved by glucose
decrease in glucose, inc in insulin, and inc in C peptide?
cortex- it contains hormones that are derived from cholesterol
medulla- makes catecholamines
what is the cortex made of?
GFR (it is also in the kidney)
what are all the hormones derived form?
they are derived from cholesterol
what does each layer make?
Reticularis- sex steroids
what is Cushing syndrome?
thats when you have excess of cortisol
how does cortisol raise the glucose levels?
it breaks down muscle for gluconeogenesis
why do patients with Cushing syndrome have muscle weakness with thin extremities?
because cortisol they act on the muscles- and that will lead to break down of muscle for breakdown and production of AA for gluconeogenesis
why do you have moon facies? buffalo hump? truncal obesity?
because you have cortisol which raises the glucose levels hence that will lead to increased amount of insulin. Large amount of insulin will lead to glucose being stored in the face, back and trunk
why do you have abdominal straie associated with cushing syndrome?
cortisol IMPAIRS the synthesis of collagen. And when you have weak collagen then blood vessels will rupture easily. so the straie in the abdomen means you have ruptured blood vessels.
cortisol upregulaes the a1 receptors on the arterioles which increases the effect of the NE.
how does cortisol have an effect on the vascular tone?
Cortisol is necessary for life- and it is necessary for increasing the vascular tone. so the way they do that is to up regulate the a1 receptors on the ARTERIOLES.
how can you have HTN associated with excess cortisol?
when you have excess cortisol-> you have excess arterioles. which will increase the effect of NE giving the patient HTN
how does cortisol cause immune suppression?
1) it leads to inhibition of phospholipase A2 and you will not make AA
2)it inhibits IL-2 which is an important T cell GF
3) it inhibits histamine- and histamine is essential for vascular permeability and vasodilation
how do you diagnose for Cushing syndrome?
24 hour cortisol levels
what happens to the adrenal glands in Cushing's syndrome due to exogenous cortisteroids?
the adrenal glands they become atrophic. when you have excess cortisol it will go to the pituitary and that will lead to the shutdown of the production of the ACTH. and that will lead to both of the adrenal glands becoming small
what are the causes of increased amount of cortisol in adrenal glands?
primary adrenal adenoma, hyperplasia or carcinoma
when would you have BILATERAL atrophy of the adrenal glands?
thats when you have hyperplasia- and that will lead to increase in the size of the adrenal gland in ONE AREA and inc amount cortisol from one area will lead to decreased production of ACTH and that will work on the LEFT adrenal gland and cause ATROPHY
what is the condition when you have bilateral hypertrophy in BOTH of the adrenal glands?
ACTH-secreting pituitary adenoma
what is paraneoplastic ACTH production what would happen to the adrenal glands?
that will lead to the increased production of the ATCH and that will hit the adrenal glands.
what is the function of the high dose dexamethosone production?
it will lead to the suppression of the ACTH production by pituitary adenoma, but it will have no effect on suppressing the ectopic production of ACTH by the small cell lung carcinoma
T/F pituitary adenoma ACTH production is SUPPRESSED by high-dose dexamethosone?
T/F high dose dexamethosone suppresses the ectopic production of ACTH by the small cell lung carcinoma?
high dose dexamethosone
what are the effects of aldosterone?
it causes increase reabsorption of Na, excretion of K/H and raises the BP
where does the aldosterone work on?
late distal tubule and the collecting duct
what are the two cells in the DCT?
principal cells and intercalated cells
what is the role of principal cells? what ions?
It leads to increase in the reabsorption of Na in the principal cells and excretion of K.
what is the role of the intercalated cells?
why do you get metabolic alkalosis?
because aldosterone acts on the intercalated cells and they lead to the excretion of H+ ions.
what are the 4 causes Hyperaldosteronism?
3. metabolic alkalosis
why do you have HTN?
because you will grab Na and that will bring water with it- and that will increase the blood volume.
what are the common causes of primary hyperaldosteronism?
it is due to the adrenal adenoma and thats when you have sporadic hyperplasia/carcinoma and they are LESS COMMON. and it is characterized by high aldosterone and low renin
what is the cause of secondary hyperaldosteronism?
it is due to the activation of the RAAS system.
when you have high aldosterone and low renin? what kind of hyperaldosteronism is it- primary or secondary?
what is it when you have high aldosterone and high renin?
what is the underlying cause of secondary hyperaldosteronism?
thickening of the wall of the blood vessel- and that will lead to the decrease in the blood flow to the kidney. or atherosclerosis of the blood flow to the kidney and that will also lead to the activation of the RAAS.
what glands are affected in CAH?
excess steroids with hyperplasia of BOTH adrenal glands
cholesterol--> pregnalone--> mineralcorticoids, cortisol and sex steroids
what enzyme is required to make mineral corticoids from (C-->P--?-->mineral corticoids)?
what enzyme is required to make cortisol?
what happens if you have 21 hydroxyls deficiency?
then pregnalone will be SHUNTED toward the production of the sex steroids and the SS will INCREASE
what is the consequence of pregnalone
CLITEROUS enlargement and precoccious puberty
no mineralcorticoids- so no aldosterone- so salt wasting (hyponatremia) and K (hyperkalemia- you are no longer excreting K), so low HTN (hypovolemic- since no Na and water comes with it)
what would happen to the adrenal glands with 21 hydroxylase deficiency?
21 hydrox- it leads to decreased production of mineral corticoids and cortisol- and so that will lead to increase in ACTH production- and that will cause bilateral adrenal hyperplasia
what is produced ALOT IN 21 HYDROXYLASE def?
what are the clinical features associated with 21 hydroxyls def?
1. salt wasting with hyponatremia
4. life threatening hypotension
5. clitoral enlargement (femaleS) or precocious puberty (males)
What is different between 11 hydroxlase deficiency vs 21 hydroxyls deficiency?
cholesterol--> (21)pregnalone--> weak mineralcorticoids--(11)> mineralcortid
what happens in 11 hydrox def?
21 hydrox- no mineral or cortisol and ALOT OF SEX STEROIDS
11 hydrox- you don't get the 2nd step of the mineral corticoids- so you only get weak mineral corticoids and SS (but NO MINERALCORTICOIDS AND CORTISOL)
what is the function of the 17 hydroxylase deficiency? what is deficient?
it allows pregnalone to enter into the cortisol and SS production
17- corteous and ss deficiecny
what is common in 17 and 11?
no production of cortisol and due to that you will have EXCESS ACTH and so there will no negative feedback and that will lead to CAH.
what is adrenal insufficiency?
lack of adrenal hormones. And it is due to the acute insufficiency and that may arise with Waterhouse Friderichsen syndrome
what is Adrenal insufficiency?
young child- N. meningitis infection. who develops DIC- bilateral necrosis of the adrenal gland- acute loss of cortisol- and that will exacerbate the HTN.
Gross- Adrenal gland that contains SAC OF BLOOD-
Adrenal insufficiency- Waterhouse Fried
what is the cause of chronic insufficiency?
1. progressive destruction of adrenal glands
2. autoimmune destruction, TB, metastatic carcinoma
where is adrenal metastatic carcinoma usually derived from?
what are the clinical features associated with adrenal insufficiency?
2. hyponatremia, hypovolemia, hyperkalemia
5. vomiting and diarrhea
where is ACTH derived from?
POMC-> MSH (hyperpigmentation)
where is adrenal medulla derived from?
neural crest derived chromaffin cells
what NT made?
they are the main physiologic source of catecholamines (E/NE)
what is the tumor of the chromaffin cells?
brown tumor- big tumor of the adrenal medulla- you will see the yellow line- and thats the adrenal cortex- and cortisol
what are the clinical features associated with pheochromocytoma?
1. episodic HTN, headaches, palpitations, tachycardia, sweating
How is pheochromocytoma diagnosed?
diagnosed by increased in serum metanephrins and increase in 24 hour urine metanephrins and VMA
what is the difference between MEN2A vs MEN2B?
MEN2A=medullary carcinoma of the thyroid, pheochromocytoma, adenoma
MEN2B= medullary carcinoma of the thyroid, pheochromocytoma and ganglineuroma of the mucosa.
what mutation is medullary carcinoma associated with?
medullary carcinoma of the thyroid- is associated with RET mutation
what is the role of VHL?
VHL- thats Autosomall dominant mutation in which you lose the VHL suppressor gene. and they will have increased risk of meningioblastoma of the cerebellum, increased risk of RCC, and increased risk of Pheochromocytoma as well
what is associated with NF type1?
Assoc. with pheochromocytoma
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