Concepts to Review Flashcards
How can Primary polydipsia present ?
-Serum osmolarity: LOW
Urine osmolality : LOW
Na+ conc. :N/Low
-Water restriction >700mOs/L (urine)
First treatment SIADH?
-**Fluid Restriction. **
-A mass in sella turcica (pituitary adenoma) indicates what?
-Either Hypo/Hyper-pituitarism.
or compression mass
Why Hypothyroidism predisposed to prolactenemia?
-It will incr TRH–>incr Prolactine
Pre-couscious puberty?
Laron Dwarfisim?
Treat?
-GH recep mutation–>LOW IGF-1 –>HIGH GH levels
-Child is not growing for age–>give mescarmine (IGF-1 analog)
NOT A TUMOR..Neg feedback*
Diffrent prognosis:
Polydypsia,Polyruia (4)
-Nephrocalcinosis,Diabetus,DI,UTI’s
In Pituitary tumor, which will be most likly elevated?
-Prolactin
Thyroid development of cells?
Parafollicular
Follicular
-4th Pharyngeal pouch
-Endoderm
Cancers that spread hematogenously?
-Hepatocellular,Follicular Thyroid, RCC
Why amiodorone causes Hypothyroidism?
-Structure similarity of Thyroid H.
Tender thyroid?
Sub acute Granulomatosis Thyroditis.
Cretisisim ass(2)?
-Abnormal development (Agenesis, dysgenesis) or Abnormal thyroid H synthesis (due to thyroid peroxidase mutation)–>Dyshormonogenesis
What a.a is the precourser for Thyroid H?
Tyrosine is made from (phenylalanine).
Hyperthyroidism can cause what special ryttm?
-A.Fib (irregular-irregular Normal QRS )
OCP use:Total T4 increases–>you have incr TBG (bounded to T4)
Cold nodules
Hot nodules
In Iodine uptake test
-Adenoma/Carcinoma
-Graves/Toxic multinodular ..
Thyroid Carcinoma mut ass
Follicular
Papillary
Medullary
Anaplastic
-RAS (bone lesions–>fractures)
-RET, RET/PTC translocation,BRAF.Most important risk factor is past radiation exposure to neck.
-MEN2A ans 2B
-Tp53
CK increase in what thyroid disorder
-Hypothyroidism
Na/k+ inactivity
Why T4 is preferred over T3?
What situation is T3 prefferd over T4?
-Better binding to plasma globulins
-T3 is acute situations.
Cytokeratin-
Von Kossa-
C. Vimentin-
D. Congo red-
E. Desmin-
Cytokeratin-Epi tumor (squamous carcinomas)
Von Kossa- abnormal calcium deposits in the body. Papillary thyroid canrcinoma.
** Vimentin**-mesenchymal tissues (endometrial carcinoma,sarcomas,RCC,Meningioma)
Congo red-Amyloidosis
Desmin-Intermeadiate filaments (Sarcoma boitroides)–>Vaginal tumor//Muscle tumors (rhabdomyosarcoma)
Patient with Hashimotos develops a rapid growing mass, what most likly diagnosis?
-B cell Lymphoma.
-Dont confuse with anaplastic carcinoma–>compression sympt.
2 important microscopic presentations of Papillary carcinoma
-Psommoa bodies and orphan annie cells.
Location od thyroglssal cyst ?
Anterior neck mass,NOT in unilateral lobe.
Mass in neck.
Pleomorphic spindle shape cell?
-Anaplastic carcinoma thyroid–>20% ass pre-excisting Follicular carcinoma.
Meaning of exopthalmus and lid retraction?
Exophtalmus is sclera visible BELOW eye lids
Lid retraction is sclera visible ABOVE eye lids.
What stimulates Insulin release indirectly(2)?
and inhibit?
- Cortisol and Glucagon
-NE and Somatostatin
What 4 H. increase in Hyperglycemia?
-Epi., GH, Glucagon, Cortisol
Most common cause of death in patients with diabetus?
-MI due to Large vessel Non-enzymatic Glycation.
When you have insulin resistance–>what does your body do (3)?
-Promotes a Incr in glucose (all H come in)
1.Gluconeogenesis 2.Protein Lysis (weight loss),3. Lipolysis 4.Glycogenolysis–> polydysia,polyuria,polyphagia,weight loss
Patient that has Random glucose of >250 presents to clinic with normal apperance. Will you diagnose him as beaing Hyperglycemic?
-NO, you need hyperglycemic symptoms.
What does somatostatin control in pancreas?
-Alpha and Beta cells secretions.
-Inhibits cholecystokynin–>steatorrhea
Gastrin–>achlorydia (abd discomfort)..
In DKA what happens to K+ and Na+?
K+ moves to extracellular space, so you may find ir elevated in serum but reality is LOW –>being excrted.Thats why we say Reduced TOTAL K+ levels.
-Hypernatremia (volume depletion).
How do you describe Gross apperance of kidney in diabetus?
-Granular pattern with cortical atrophy
What is Insulin and C-Peptide level in Type 2 DM?
-Depends.They can be both increase or both decreased.
How to differentiate
17 alpha Hydroxylase
11 alpha Hydroxylasse
21 alpha Hydroxylase
Aromatase
Desmolase
-Only one with decr Sex H. (Female assymptomatic until puberty–>Amenorrhea)
-Incr BP and Decr K+ serum (11Deoxycorticosterone)
-Low BP and High K+ serum
-No electrolyte abn (K+ normal),Norml BP.
-Fatal
What does Cortisol do to FSH and LH?
-Where is it seen?
-Cortisol messes with GnRH secretions--> leads to *mesntrual irregularity (80%) *,amanorrhea,oligo.
Hirsutism, erectile dysfunction.
-Seen in Cushion syndrome.
Diagnosis
Patient untreated and has Graves and presents with infection–>develops Agitation,Confusion and Tachyarrythmias?
-Thyroid storm.
-4P’s
Are hot nodules malignant?
-Rarley
Patient with thyroid cancer opts for a total thyroidectomy. Weeks later, paresthesias and hyper-reflexia develop. What happened?
Removal of parathyroid glands–>HYPOCALCEMIA
Most comm cause of HypoPTH is (3)
-Thyrodectomy. AIRE mut (autoimmune), Di-George syndrome.
-Spasm,parasthesia,Tetany
Diagnosis
Low Ca++ levels,Short 3 and 4 digits,Dvelop delay and short stature??
-PseudoHypoPTH
Where does PTH act?(3)
1.PCT (Na/Phosphate transporter)
2.DCT (Na/Ca++ Co-Transporter)
3.Osteoblast–>incr RANKL rel–>stimulates osteoclast.
Diagnosis
Hypercalcemia
Hypophosphayemia
Hypercalciuria
-Excessive urination ,constipatin, flank pain , pain in bones ,and feeling depressed.
Complication??
-Excessive urination (Polydypsia)(Thrones),constipatin (Grones), flank pain (Stones), pain bones (Bones), and feeling depressed (psychyatric overtones)
-HyperPTH
-Osteitis Fibroda Cystica( made up of Hemossiderrin + Fibrous tissues) “Brown Tumor”
-Most commm cause of Primary PTH,Secondary PTH??
-How to differentiate between Secondary HyperPTH between CKD and other and what complication may arise??
1= PTgland adenomas and SCC,RCC
2=CKD
-CKD–>HyperPHOSPHATEMIA (NO kidney function) +Hypocalcemia
Others: Hypophosphatemia
-Complication: renal osteodystrophy–>BONE LESION.
Diagnosis
pins-and-needles,” burning, tingling, and numbness in the distal extremities,temperature sensation, decreased vibratory sensation, and proprioception. Deep tendon reflexes are also diminished
-DM
What is ass with Diabetic neuroptahy.
**Autonomic neuropathy **associated with diabetic neuropathy may result in *postural hypotension, arrhythmias, abnormalities of sweating, nocturnal diarrhea, gastroparesis, impotence, and bladder dysfunction. *
What values constitutes microalbuminemia in urine in Diabetus mellitus??
-30-300mg/dL
Mechanism on INSULIN
GH/IGF-1
Epi/NE
-Promote Insulin resistance,by decr glucose uptake
-In Glucagon
Most used values for kidney Diabetus damage??
-Albumin:creatine ratio.
What happens to K+levels in both DKA and HHS?
-DKA: Incr Extracellular K+ –>Total K+ loss(Ketones presents)
-HHS:Incr Intracellular K+ (NO Ketones)
What is it?
Basement membrane thickening and protein leakage lead to nodular glomerulosclerosis and progressive proteinuria
Diabetus progression to Chronic Renal disease.
hat is the consequence of small vessel disease in individuals with chronic diabetes mellitus in the retina?
Diffuse basement membrane thickening causes retinal hemorrhages, vessel proliferation, microaneurysms, and exudates
3 common causes of Hypoglycemia in DM
1.Toxicity of Insulin secretants
2.Excessive exercise
3.No food intake while taking medications.
Cortisol functiona?
-Maintains BP
-Stops division of Immune cells(Immuno supressors)
-Blocks neutrophils migrationn–>Neutrophilia
-Decr NFKB–>reduces TNF alpha,Lipoooxygenase, COX2.
-Incr glucose production in liver + reduces uptake in peripheral tissues.–>Diabetogenic effects.
-Incr lipolysis–>High cholesterol levels
-Decr bone formation (incr risk of fractures–>osteopenia/osteoporosis).
-Decr fibroblast–>poor wound healing–>thin skin (striea)
-Promotes adipocyte growth in central part of body.
What 2 serum vamues are associated with Cushion syndrome beside cortiso and ACTH??
Hyperglycemia and Hyperchlomeria
Diffrence treat of 1* and 2/3 adrenal insufficency??
-What do you see that RX dosent tell you?
-1–>need minerolocorticoid
2–>dont needed
3*–>glucoccorticoid abrupt stop
Hypoglycemia**
Patient with low cortisol develops sepsis??
Addison crisis.Ass with meningiococcemia and bilateral adrenal hemorrage.
Causes of 2* Hyperaldosteronism??
-Juxtaglomerular tumor (secrete renin), renovascular disease, CHF,Cirrosis,Nephrotic syndrome.
Conn syndrome?
Primary Hyperaldosteronism (adrenal tumor)
How do differentiate between 1 and 2 Hyperaldosteronsim?
-Differentiate due to Renin levels. amd given ACHE Inhibitor.
-Primary you do not have edema (Persistant Aldosterone escaoe mechanism)
What are 4 hormones in Pheochromocytoma?
-Ass mutations?
-Epi,NE,Dopamine,EPO.
-VHL and MEN2A and 2B
Vasoactive Intestinal Peptide Function??
Normal functions of VIP include increased secretion of water and electrolytes into the intestinal lumen and relaxation of intestinal smooth muscle and sphincters.
What hormone out of 4 stress H (Glucagon,Epi.,GH, and Cortisol) does proteolysis?
Cortisol (loose weight).
Why in Congenital Bilateral Hyperplasia codnitions all have bi lateral hyperplasia?
-Cortisol defc.–> ACTH incr–>Hyperplasia.
Sympt. of Pheochromocytoma but empty medulla.Explanation
-Extra-adrenal (bladder,mediastainum).Do test to detect.
-Panic attacks is differential.
organ of Zunckerkandl??
-Pheocrhromocytoma extra-adrenal in bifurcation of aorta.
Diffrence between Pheochromocytoma and Neuroblastoma in amount of H produced?
-Pheochromocytoma= lots of cathelcolamine–>see them in urine.
-Neuroblastoma= inmature cells,dont see them in urine that much.
What is Gestational diabetus??
-Mother has Diabetus Type 2–>Hyperglycemia–>passes it to fetus and fetus responds by HYPERPLASIA of Beta cells–>Hypoglycemia
When symptoms of Type 1 DM start to appear and what do you see before sympt appear in microscipic image of pancreas?
-Start appearing after Beta cells are completly destroyed–>Insulin is normal.
-Before they are destroyed you see INSULINITIS
What do you see in PTHgland-carcinoma?
-Ca++ levels are so high you definitly see Arrythmias.
What mutations id Toxic mediated nodular Goiter ass??
TSH recep mutations. (60% cases).
Why do patients with follicular carcinoma thyroid may have incr Iodine uptaje in other parts of body??
-This tumor metastasisez to bones and lungs–>expect Incr Iodine uptake in this regions.
Diffrence of 1* and 2* adrenal insufficency?
1*–> Adrenal inflamation (AIRE) and TB (resource pour countries)
metabolic acidosis, Hyperkalemia, LOW BP, Hypoglycemia, Hyperpigmentation
2/3–> Low ACTH secretion (compression adenoma or hypopituitarism)
Aldosterone is spared–> Hypokalemia,NO hyperpigmentation
Why you don’t need aldosterone treat.
Why dysgenesis of thyroid in neonte dosen’t present with sympt?
-Mother has “passive immunity” towards child.
What happens to TSH and T3 when giving amiadorone?
-Amiodorone mimmics T4 and inhibits 5’diodinase–>DECR T3 and INCR TSH
What test do you do to diagnose Acromegaly?
-Oral glucose tolerance (72g within 2hr. it should supress it)
Whats the classic triad of pheochromocytoma?
-Sweating,Tachycardia and headaches episodic.
**Hypertension <20yrs–>think Pheochromocytoma*
Steps on diagnosing Cushions syndrome?
How to differentiate between Ectopic and Pituitary ACTH tumors physically?
- Do 24hr. urine cortisol, salivary night test, or LOW dose dexamethasone overnight.Just need 1 to determine Cushion (high cortisol).
- ACTH levels
- If ACTH is high–>HIGH dose Dexamethasone test.
-Ectopic has NO ACTH secretion.–>related peptide is decr (MSH).
**-Adrenal Cushion low ACT **
What happens in preganacy to TSH, T4 and TBG?
TBG Incr
T4–>Incr
TSH–>decr.
hCH has similar alpha subunit–>esxplains
-Estrogen incr TBG
Why do you see Hyponatremia in Hypothyroidism??
-Decr CO–> leads to ADH secretion–>fluid retention which may lead to hyponatremia
From where does rT3 derive?
-From T4
-Both rT3 and T3 derive from T4.
-In hypothyroidism rT3 and T4 and T3 wiil be decr.
What does excessive cortisol cause?
HyperTG, Hypercholesterol, Hyperglycemia, HyperBP,Immunosupression,Osteoporosis,Amonorrhea.
What Thyroid Cancers are most likely to have hot nodules?
-The ADENOMAS
-Carcinomas are always cold nodules.
Common presentation in patient with AIRE mut affecting parathyroid glands? What other endocrine abn may be present along side?
-Recurrent mucous-cutaneous candidiasis
May be ass with Addison disease.
Minerocorticoids defc-->hypotension,salt graving,hyponatremia
Glucocorticoid defc–>lowBP,fatigue,hypoglycemia,
Androgen defc.-->delayed pubic and axillary hair growth
Loose Total Body K+ in what Diabetic emergency?
-BOTH
VIPOMA explanation
-Promotes secretion into intestinal lumen–>excessive watery diarrhea every** even when fasting—>LOW BP**
-Also causes excessive K+ and Cl- secretion–>**Hypokalemia **and Hopychloremia.
-Incr bone resorption–>Hypercalcemia and Hyperglycemia.
What does CK enzyme do?
**-Phosphorylates creatinine via taking Phosphate form ATP–>forms creatine-Phosphate—>stored for energy. **
Granulomatous inflamation with multinucleated giant cells engulfing colloid
subcutaneous Granulomatous (Tender)
What is Euthyroid sick syndrome?
How to diff with central hypothyroidism??
Do you treat??
-When a patient has a infection (non-thyroid related condition) and presents to hospital and when mesuring thyroid levels you see:LOW TSH, low T3, HIGH rT3.
**-Don’t treat it. Patient has **–>completly normal.
Central hypothyroidism and euthyroid is differentiated by rT3 levels, where normally rT3 will follow T4 levels.But in euthyroid it won’t.
-Very common to see it in hospitals.
What other conditions is ass with MEN2B aside form medullary and mucosal neuromas?
-Marfan Habitus–>NO risk factor for aortic root dilation or ant **lens dislocation. **
Usual presentation of Conn syndrome?
-Hypertension, Low renin, High aldosterone
Weakness (low K+), NO edema (Na++ inside BV dosent let H2O move outside), metabolic alkalosis
Whats the mechanism of Aldosterone escape?
-As atrium fills and BP rises due to excess Aldosterone–>ANP is rel to eliminate excess water–>NO edema
