Renal Endo GU Flashcards
Oligohydramnios
Potter’s Sequence: Lung hypoplasia, flat face/ears, limb defects.
Pre-renal azotemia Labs
Increased Serum BUN:CR > 15. FeNA<1%, normal Urine Anion gap, high urine osmality (kidneys are working)
Post-Renal Azotemia Labs
Initially you get absorption of BUN (cuz tubules are working thus BUN:CR 15. FeNA>2%, (cuz kidneys have broken)
Intrarenal injury labs
Elevated BUN and Cr (decreased GFR) thus Serum BUN:CR < 15. FeNA>2%, (cuz kidneys have broken) and no urine anion gap
Ischemic ATN location?
Proximal tubule and Medullar segment of ascending limb
Nephotoxic ATN location and causes?
-Proximal Tubule -Aminoglycosides, heavy metals, myoglobin (crush injury), ethylene glycol, radiocontrast
Eosiniphils in urine?
Acute interstial nephritis leading to Acute renal failure. Drug induced: PCN, NSAIDS and diuretics
Gross Hematuria and Flank pain?
Renal Papillary Necrosis. dt progression of acute interstial neprhitis. From Long term analgensic use, DM, Sickle cell trait, severe acute pylenephritis
Nephrotic Syndrome Presentation
Edema, infeciton, coagulation, poor lipid profiles from: Hypoalbunimemia, hypogammaglobulinemia, hypercoagulable state (loss of ATIII), hyperlipidemia and hypercholesterolemia (“liver trying to compensate for thin blood”)
First and second most common renal issue in SLE?
1) Diffuse proliferative glomeruloneprhitis 2) Membranous nephropahty
Renal diseases with granular immunoflourecence?
Immune complex deposition: (look for word membranous) MGN, MPGN
Puffy face in kid?
Minimal Change disease (losing albumin but no IgG due to cytokine induced effacement of podocytes)
Focal Segmental Glomerulosclerosis is associated with which populations? Positve or negative immunoflourescence?
AA, Hispanics, HIV, Herion, sickle cell disease. Negative immunoflor.
Spike and dome appearance? Where? Condition associated with?
1) Membranous nephropathy. Subepithelial side of BM. Immunocomplex dep. 2) Hep B/C, solid tumors, SLE, drugs.
Tram Track appearance? Location?
1) MPGN Type 1 > Type 2 (2 associated with C3 nephritic factor stabilizing C3 converatse = compliment acitvation). 2) Type 1 (Subendo); Type 2 (BM)
Diabetic Mechanism of Renal Damage
Non-enzymatic Glycosolation of BM allowing for hylanie arteriolosclerosis. Preferentially of efferent arteriole leading to hyperfiltration injury.
Round lesions in glomeruli? Associated with which condition? Other findings?
Kimmelstein Wilson nodules (christmas ball sclerosis) in DM. Increased PAS+ staining eosinophilic material.
Mechanism for general nephritic syndromes?
Immune complex deposition activating C5–>C5a which attrachs neutrophils causing hypercellular inflamed glomerulus
Child who was recently sick with throat infection, has risk for what renal disease? Virulence factor? Histology?
Post-strep glomerulnephritis. Group A beta hemolytic strep (pyogenes) with M protein factor (M causing N-ephritic). Supepiethelial humps
Cresents on histology indicative of? Made of what?
Rapidly progressive glomeulonephritis. Made up of inflammatory debris (macros and fibrin).
Family with hearing, vision, and hematuria
Alport syndrome, X linked, defect in Type 4 collagen. “Can’t see, can’t hear, can’t pee)
Bugs in cystitis
E coli. Staph Saprophyticus (in young sexually active females, novobiocin resistant)
Fever, flank pain, wbc casts, leukocytosis
Pyleonephritis. Ecoli, kleb, enterococcus faecalis
Cortical scarring with blunted calyces.
Chronic Pyelonephritis. Can also show thyroidization of kidney from eosinpholic proteinaceous material with waxy casts in urine
Calcium oxalate/phosphate stones: causes and tx?
Idiopathic hypercalcuria, hypercalcemia, crohns. Tx with HCTZ (calcium sparing diruetic; but increased risk of gout with HCTZ).
Ammonia Pyrophosphate Crystals (AMP stones)
PPPS: proteus, high pH, pyrophophates, staghorn coliculi (nitus for UTIs). Kelbseilla too cuz its also urease positive.
Uric Acid Crystals
Radiolucent, “U CAN’T SEE U-RIC Cystals”. Gout. Tx: alkalinize urine and allopuirnal + hydration
Where is EPO made?
Renal peritubule epithelial Cells
Hematuria, palpable mass, flank pain
Renal cell carcinoma.
Presents with Left sided varicoceal, Paraneoplastic (EPO, PTHrP, ACTH). Loss of VHL or gene deletion (BOTH ON CHROMO 3)
Obesity/smoking is risk factor.
Mets to retroperitoneal lymph nodes, but “prefers” IVC hematogenous spread
Hemangioblastoma of Cerebellum and Renal Cell carinoma. Chromosome? Associated with?
vHL. Chromo 3.
Panc NETs, Pheos
Wilms tumor, neonatal hypoglycmie,a muscular hemihypetophy, oragnomegaly (tongue)
Beckwith wiedemann syndrome
RCC and HCC will can be associated with?
EPO production leading to 2dary PV or ANEMIA OF CHRONIC DISEASE (iron def anemia=microcytic)
HPV Subtypes: High risk? low risk? Vaccine Covers? High risk virulence factors?
Low Risk: 6, 11 forming condylomas. High Risk 16 18 31 33: squamous cell cancer particularly of transformation zone of cervix (also causes Adenomas) Vaccine: 6, 11, 16, 18. (therefore still need PAPs for other subtypes). E6–l p53; E7–l Rb–l E2f–>G1 to S phase transition
DD for Extramamillary Paget’s disease? Markers for each?
Carcinoma (Keratin +, PAS +) Melanoma (S100+; comes from neural crests) However usually there is no underlying cancer as opposed with Paget’s Disease of Breast
Focal Persistence of columnar cells in upper vagina? Exposure? Risk for? Embryologic Derivatives?
Adenosis (different than Adenomyosis). Embyologically the lower 1/3 (from urogenital) sinus starting as squamous cells. These during maturation normally overtake the upper 2/3 columnar cells (from mullerian duct). DES exposure in utero causes persistence of columnar cells putting pnt at risk for CLEAR CELL ADENOMA.
Bleeding Grape like mass on genitals of <5yo? Dx tests? Histological Features?
Embryonal Rhadomyosarcoma. Desmin +, Myogenin +. Cytoplasmic Cross Striations present.
Post-coital bleeding in a middle aged woman?
Cervical Carcinoma (increased risk w/ smoking; invades locally=likely to cause hydronephrosis leading to ARF).
Amennorehia in woman who recently had a choriocarcinoma
Asherman’s Sydnrome of uterine adhesions causing secondary ammenorhia from overagressive Dilatation and Cuerrtetage causing a loss of uterine basalis (no stem cells to regen endometrium)
Abnormal uterine bleeding of woman on tamoxifen
Uterine polyp, side effect from tamoxifen stimulating endometrial ER (antagonist in breast, agonist in bone=osteoprotective)
Severe cyclic pain in female cycle? Features?
Endometriosis (glands and stroma outside of endometrial lining). Chocolate cysts (walled off cyst without outlet for blood to escape), gunpowder lesions (endometrium in soft tissue)
Endometrial glands and stroma in the muscular layer of uterus
Adenomyosis (different than adenosis)
Anovulatory Cycles put pnt at risk for?
Endometrial hyperplasia progressing to dysplasia (from unopposed estrogen=growth; no progesterone=no cycling)
Endometrial Carcinoma. Pathways? Age group? Mutations?
1) Endometrioid (Type1): hyperplasia from unopposed estrogen leading to dysplasia. 50yo, PTEN mutation, obese women. 2) Sporadic (Type2): Papillary Serous (psammoma bodies), Elderly/frail, p53 mutation
Mutiple white whorled masses on endometrial biopsy
Leiomyoma (fibroids), bening no risk to progression. Minor risk for infertility. Presents in young female
Single mass on endometrial biopsy
Leiomyosarcoma. Usually postmenopausal, irregular, necrotic, arrising de novo****
Obese young woman with infertility oligomenorrhea, and hisutism
PCOS: increase LH>FSH ratio (2+; meaning increased androgens which cause male fat distrubution, hair, and ammenorhea=aromatization in hypothal to E2 which shuts down HPgondal axis)
Ovarian Tumor in: 1) 15-30yo 2) 35-40yo 3) 60-70yo
1) Germ Cell Tumor 2) Benign surface epithelial tumor 3) Malignant surface epithelial tumor
Single Ovarian Cyst
Benign Cystadenoma (30-40yo), smooth lining
Multiple Ovarian Cysts
Malignant, Shagy lining, postmenopausal women
BRCA1 carrier at risk for?
Breast, Endometrial, Fallopian and Ovarian (serous). Why angelina jolie went for hysterectomy with bilateral salphingooorphorectomy.
Ovarian tumor with urothelium
Brenner Tumor (B for bladder-like=urothelium)
Where do ovarian tumors spread?
Seeding of peritoneal cavity, Omental caking
Tumor marker for ovarian cancer?
CA-125 (used to monitor response to therapy/recurrence; NOT SCREENING)
High AFP and betaHCG (female)
Embryonal Carcinoma (germ cell tumor). “malignant teraatoma”
AFP (female)
Endodermal Sinus Tumor (yolk sac tumor): “YAFP”, yolk is yellow like urine=schiller duval bodies (renal glomeruloid bodies in tumor)
LDH, Alk phosph and Large cell with clear cytoplasm (female)
Dysgerminoma, malignant
High BetaHCG (female)
Choriocarcioma
Small eosinophilled fluided between granulosa cells.
Call-Exner bodies indicative of granulosa/theca cell tumors. Pnt will have estrogen excess=precocious puberty or abnormal cycles or postmenopausal bleeding.
Pleural Effusion and ascites associated with tumor? (female)
Meigs Syndrome: triad of fibromas, ascites, and hydrothrorax.
Women will note pulling sensation in groin
Pink Crystals found in tumor (female)?
Reinke Crystals, Sertoli/Leydig cell tumor: Excess andros producing hirtuism/virilization
Bilateral ovarian tumors with nuclei pushed to side in cells
Krukenberg Tumor (GI met), mucus producing signet cells.
Female presents with mucinous distension of stomach
Pseudomyxoma Peritonei (jelly belly); udt mucinous adenocarcinoma of appendix
Woman comes in with abdominal pain what test?
PREGGERs TEST ALWAYS
Woman with history of DVTs and spontaneous abortions
Antiphospholid Antibodies/Lups anticoagulant (antibodies to ATIII)
Placenta seen on preg cervical examination
Placental Previa; risk to cut blood supply during labor therefore C section indicated
Severe Bleeding during 3rd trimester
Placental Abruption, risk of DIC (amnoitic fluid is high in thromboplastin), and Amniotic fluid Pulm Embolism.
Placenta implanted in the wrong tissue?
Placenta Accrete (A for adhesion) into the myometrium (rather than the functionalis layer). “Increta” for insertion (little worse) “Pecreta” for penetration (much worse)
Fibrinoid necrosis of placental vessels?
Preeclampsia. HTN, proteinuria, edema in 3rd*** trimester. Risk to progress to eclampsia = seizures.
Preggers with anemia, and abnomral LFTs
HELLP: Hemolysis, Elevated liver enzymes and Low platelets.
High BhCG with larger than normal uterus at gestational landmarks
Hyatidiform mole; risk of Choriocarcimona; passing of grape like masses, snowstorm appearance on Ultrasound. Monitor BhCG levels to rule out choriocarcinoma.
Types of Choriocarinoma?
Complete: 46 chromos, all from dad, highest BhCG, higher risk of choriocarcinoma (will respond to chemo better than sporadic chorios). Partial 69 chromo (46 from dad), Less risk for choriocarcinoma.
ACEI’s SEs?
CATCHH: Cough, angioedema, teratogen, creatinine increase, hyperkalemia, hypotension
von Hippel Lindau
Autodominant, Capillary hemangioblastomas in Cerebellum and Retina, congential cysts, neoplasms of the liver, kidney (bilateral RCC), pancreas
Osler Weber Rendu
Hereditary Hemohorrage Teleangectasias: autodominant, epistaxis, GI bleeding or hematuria
Sturge-Weber Syndrome
Encephalotrigemnal Angiomatosis: Neurocutaneous disorder: facial and leptomeningeal angiomas. Skull radiagraphs can show tram track appearance.
Which ligament does a surgeon ligate during an oorphectomy?
Suspensatory Ligament (infundibulopelvic ligament)
Breast Milk Deficient in?
Vit D and K (both fat sol…dunno why tho). DK
What measures are reflexctive of the following
Urea
Creatinine
PAH
Urea: reflective of water absorption of kidney. When a person is dehydrated urea increases from holding onto water. (increased BUN:CR in dehydration=prerenal azotemia)
Creatinine: Freely filters and additonal 10% secreted by prox tubule. Increases in only creatinine signify renal failure as there is less filtration and this extra 10% Cr stays in blood (not secreted).
PAH: tells you renal plasma/blood flow as it is has almost a 100% clearance (both freely filtered AND secreted)
DD between Leydig Cell hyperplasia and Congential adrenal hyperplasia?
Both show early virulization:
Leydig cell WONT show increase in 17-hydroxyprogesterone levels
21 alpha hydroxylase def will show increase 17 hydroyprogesterone (and both show inc testoterone). Can show salt wasting (severe form) but doesn’t have to (moderate form)
Difference between IgA nepropathy and PSGN?
IgA Nepropahty presents several days after the infection. Compliment levels are normal. Mesangial Deposition will be seen on EM.
PSGN takes a FEW WEEKS to devo. C3 is low**
Two things that relax uterine tone?
Increase?
B2 agonists and P4
Oxytocin, and PGs
Cirrhosis/Liver Failure’s Effect on male?
Decreased break down of estrogens causing hyperestrogenemia==Gynecomastia/spider angiomatas
(not verified but) this causes increased sex hormone binding protein production (questionable cuz of liver failure) which further decreases testosterone causing erectile dysfunction.
Where does the fructose come from in seminal fluid?
Seminal Vessicles
Renal Failure’s Effect on Bleeding? Why?
Hyperuremia causes platelet qualitative dysfunction of platelets.
Normal PT/PTT and normal platelet levels
IgG4 Antibodies to phospholipase A2 (PLA2R)= transmembrane protein on podocytes results in what form of kidney disease?
Membranous Nepropathy
PSNS and SNS control of insulin secretion?
Smell/sight of food=PSNS driven insulin secretion
SNS: Alpha’s inhibit insulin secretion, Beta stims insulin secretion
What does Thyroid Peroxidase do?
Iodinate Thyroglobulin
Severally dehydrated patient, where is majority of water resorbed?
Proximal Tubules (60% of water) NOT proximal and distal collecting ducts (this aids via ADH but majority still in Prox tubules)
What hormones share the same alpha subunit?
TSH, LH, FSH, betaHCG
Cancers that cause ectopic:
ACTH
PTHrp
EPO
ADH
1) Small Cell carcinoma
2) Squamous cell carinoma of lung, breast, renal cell carcinoma
3) RCC, HCC, hemangioblastoma, Pheos
4) Small cell carcinoma
Insulin Receptor?
Tyrosine Kinase inducing glucose uptake via increased production and expression of Glut transporters.
Also turns on Na/K atpases
Insulin dependent and independent Gluts? And where are they found?
GLUT 4: Dependent; Adipose and skeletal muscle
GLUT1: Independent; RBCs, brain cornea
GLUT5 (fructose): indepent spermatocytes, GI tract
GLUT2 (bidirectional) indpendent: b islet, liver, kidney, small intesine.
Hormone cause of insulin resistance?
GH
Increased FFA in serum—mechanism unknown
Insulin release in Beta islet cells?
Glucose enters GLUT2
Glycolysis generating inc ATP:ADP
ATP closes ATP-senstiive K channels
Cell depolarizes bringing in Ca
Ca causes granular release of prepackaged vessicles of insulin
Most specific sign for hypercortisolism? and mechanism?
Vilaceous Striae.
Cortisol inhibits fibroblast activity
Wolff Chaikoff effect?
Excess Iodine temporarily inhibits thyroid peroxidase causing decreased iodine organification lowering T3/4 production
How does T3/T4 get into cell?
T3/T4 are lipophilic but still use ATP membrane dpeendent transport
Child presents with abdominal distension and a firm irregular mass CROSSING midline. Dx?
Other associations?
If it didn’t cross midline?
Neuroblastoma (can be anywhere along sympathetic chain), most common extracranial childhood cancer of neurotissue
Neural Crest origin. HVA in urine. Bombesin +, N-myc oncogene.
Opsoclonus-myoclonus syndrome: non-rhythmic conjugate eyemovement (WONT SEE THIS IN MEDULLOBLASTOMA)
Homer-right rossettes can be associated (radial arrangments of tmr cells surounding fibrils)
(Wilms tumor if it didn’t cross midline)
Child with large abdomen, puffy face, and large tongue, with some signs of mental slowness
Cretinism (congential Hypothyroidism)
6P’s Pot biellied, pale, puffy faced, protruding umbilicus, protuberant tongue, poor brain devo
Increased ESR, jaw pain, Tender thyroid
De Quervain subacute thyroditis
usuually following a flu, self limited
De querVAIN’s has PAIN
Granulomatous inflammation
Thyroid replaced by fibrous tissue
Riedel thyroidits
Hard rock like painless thyroid(“hard thyroid like riddell helmets”)
Need to DD this with anaplastic carncoma
Cuase of toxic multinodular goiter?
Mutation in TSH receptor causing hyperfunctioning follicules. “HOT NODULES” rarely malignant
MHC associated with Hashimotos?
HLA DR5
“Thive-roid”
Thyroid Storm Tx?
3 P’s
Propanolol (Bblockers), Propylthiouracil, Prednisolone (corticosteroids)
Beta blockers are used because T3 upregulates beta receptors (particularly in heart) leading to SNS type sxs commonly seen in hyperthyroidism
NB: Steroids are the only thing that will decrease proptosis rapidly…Propylthio/meth won’t
Thyroid cancer associated with:
Psammoma bodies
RET mutation (2)
MEN2a/2b
Older Patients
Childhood irradiation (eg eastern european)
Hashimoto’s
Empty appearing nuclei
Amyloid stroma with sheets of cells
Psammoma bodies: Papillary
RET mutation (2): Papillary (also associated w/ BRAF), Medullary
MEN2a/2b: Medullary
Older Patients: Anaplastic
Childhood irradiation (eg eastern european): Papillary
Hashimoto’s: Lymphoma (nonhodgkins)
Empty appearing nuclei: Papillary (annie orphan nuclei)
Amyloid stroma with sheets of cells: Calcitonin secreting cells=Medullary
Increased cAMP in urine?
Hyperparathryoidism (usually primary)
How to Dx acromegaly
Increased Serum IGF-1
or Failure to suppress GH following oral glucose tolerance test (normally: Glucose–l GH)
Pituitary mass on MRI
Dx ZE syndrome?
Secretin injection
nonZE: Secretin—lGastrin
ZE: secretin—>Gastrin (wont inhibit it)
POMC cleaved into?
ACTH, MSH, and Beta endorphin (opiate type molecule)
Rubber Factory Worker with hematuria? Other risk factors for this condition?
Transitional Epithelial cancer of the bladder
Cyclophosphamide, smoking, aniline dyes, phenacetin,
NB: Schistosoma is associated with SQUAMOUS CELL CARCINOMA
Where does the following estrogens come from?
E2
E3
E1
E2: Ovaries
E3: Placenta
E1: Adipose Tissue
Hypothyroidism can result in what two endocrine related outcomes?
Lactation and Amenorrhia
Extra TRH stimulates PL release which can inhibit GnRH.
Addisons Disease
Cushings Disease
A-ddisons is primary A-drenal Insufficiency
Cushings is pituitary ACTH overproduction
Drug to give if aldosterone deficient?
Flucortisone
HCTZ SEs?
“hyperGLUC”
Hyper:
GLYCEMIA, LIPIDEMIA, Uricemia, Calcemia,
Hypo:
Kalemia, Tension
Patient being medically treated successfully for hyperthyroidism, now comes to your office with fever and throat pain. What do you do?
Get a WBC count and differential as both Propthiourical and methimazole have AGRANULOCYTOSIS as a SEs.
PTU also block 5’ deiodinase peripherally
Methimazole is teratogenic
Branchial Cleft cyst vs Thyroglossal duct cyst
Thyroglossal Cleft cyst moves with swallowing and is medial (remove cuz of risk of infection)
Branchial Cleft cyst is lateral and doesn’t move with swallowing
What AA precursor does thyroglobulin come from?
Tyrosine. MIT=MonoiodoTyrosine
Most common lab values of someone with hyperthyroidism?
Low TSH high T3/4
Graves disease
C peptide levels reflect?
Endogenous insulin.
High insulin without C peptide=means exogenous delivery
Leptin stims and inhibits?
Leptin Inhibits Lateral Hypothalm
Stims Ventromedial Hypothal
Thus it is a satiety signal
Metabolic Syndrome Criteria
3 of 5:
Low HDL
High BP
High Fasting blood glucose
High TAGs
Abdominal Obesity
DIffernce between Renal osteodystrophy and other secondary hyperPTH?
Renal osteodystrophy will present with HIGHER PO4 from nephron loss being able to respond to PTH’s signal to dump PO4.
While most other secondary etiologies will show lower PO4
One potential cause of maternal diabetes. Hormones effect?
hPL: human placental lactogen from syncytotrophblasts.
Has both Prolactin and Growth Hormone (insulin resistance) function
Placenta also contribues with GH, Estro, Progestro and glucocorticoid production
Blocks sodium iodide symporter on basolateral membrane of thyroid follicular cells?
Potassium Perchlorate.
Can be used in patients who are refractory to PTU/Meth. This will inhibit iodine uptake and lower the amount of iodinated thyroglobulin availible to be released.
What do following cells do/location:
JG Cells
Macula Densa
JGApparatus
JGCells: SYSTEMIC BP control. On afferent arteriole and monitor Bp thus affecting afferent vasoconstriction which maintains adequate total BP to kidney. If bp is decreased they secrete renin increase body bp.
Macula Densa: of Distal convuluted tubule. Monitor resorption of kidney via [Na]. High [Na] means high flow (less time to resorb Na). Thus low [Na] means low flow (more resorb time) which means low BP causing RENIN secretion
Fanconi Syndrome? Location? Sxs?
Resorption defect in prox convuluted tubule. (severe RTA type 2)
Heridtary defects (Wilson disease), ischemia, nephrotxins/drugs
Renal tubular defects?
“FABulous Glittering Liquid”
FAnconi Anemia: Prox tubule, RTA2
B-artter syndrome: thick ascending loop, hypok + meta alk + hyperCa (think HCTZ, despit dif location of action)
Gitelman-poor resorb of NaCl in DCT (hypoK, met alkalosis, NO hyperCa)
Liddle Syndrome: Distal collecting duct (increased Na resorb): HTN, Met alk, dec aldo
NSAIDs effect on kidney?
Inhibits PG’s (loss of afferent vasodilation) causing:
Decreased GFR and Risk for ischemia causing acute renal failure
Easy way to remember renal pathologies with Type III HSR?
They will have “itis” in their name.
PSGN, Diffuse proliferative glomulonephritis, Membranoproliferative glomerulonephritis, Membranous glomerulonephritis
Dysuria and hematuria in several boys at day care?
Adenovirus causing hemorrhagic cystitis.
SEs of Glitazones?
What patient don’t you use metformin in?
What patient don’t you use sulfonyureas?
Hepatoxicity, Heart Failure, Weight gain.
Renal failure cuz of risk for met acidosis
DM1 cuz you need some functioning Beta cells to have an effect
Treatment for Esophageal Varices? What else does this drug treat?
Octreotide (somatostatin analog).
Acromegaly, carcionid, gastrinoma, glucagonoma
Furosemides Mech of Action (2)? Where?
SEs?
1) Inhbits NaKCC2
2) Stimulates PGE** release–>vasodilation of afferent arteriole increasing diruresis.
**NSAIDS inhibit this—thus NSAIDs inhibit Furosemide’s efficacy
3) Thick ascending limp of Loop
4) “DANG furOHsemide”: Dehydration, allergies (sulfa), Nephritis (interstitial), Gout***, Ototox, HypoK (and hypoCa)
Fluid in body proportions?
“60 40 20”
60% Total body water
40% of Total body weight=Intracellular fluid (High K)
20% of Total body weight=Extracellular fluid (high Na): of this 1/4 (5% total fluid) is plasma volume and 3/4 (15% is interstitial fluid)
Plasma is about 5% of total body weight**
Where does PTH cause Ca absorption in nephron?
Early Distal convuluted tubule.
2 things that turn on Na/K atpase?
SNS tone (B receptors) and insulin
both lowering K levels/causing hypokalemia
Electrolyte disturbance giving decreased deep tendon reflexes?
Hypermagnesemia
Nephrogenic DI tx?
Tx for lithium induced DI?
1) HCTZ–diruretic is forcing tubules to hang onto water
2) Amiloride for lithium induced DI; NB HCTZ will cause lithium TOXICITY (decreased excretion)
Waxy casts in urine?
Fatty Casts?
End stage (advanced) chronic renal disease
Nephrotic Syndrome
Fever Rash eosinophilia, azotemia?
Drug Induced acute interstitial nephritis
tx w / steroids
Chronic Acetaminophne use causes what renal issue?
Other risk factors?
Renal papillary necrosis.
DM, Acute pyelnephritis, sickel cell anemia AND TRAIT (renal papilla have very low O2 tension thus increased risk of sickling causing vasocculsive crisis)
Dehydration with NSAIDs puts patient at risk for?
Acute Renal Failure from decreased renal perfusion
NSAIDs stop afferent arteriole PG mediated vasodilation.
Why do you see pseudohyperaldosterism in cushings?
Cortisol has weak mineralcorticoid activity and is normally inactivated by local 11betaHSD2. But in cushings this enzyme is overwhelmed and so you get mineralcorticoid activation.
Levels of ACTH in Primary Hyperaldosterism? Why?
Aldosterone Levels in secondary/teritary hypoadrenalism?
1) Normal. Aldosterone feedback is at the level of kidneys (knocking down renin) and isn’t part of the HPA axis
2) Secondary/tertiary means bad pit/hypothal thus no on signal to adrenals. Will have normal levels of aldo because renals are intact so they can stimulate Glomerulus of adrenal cortex
When do you have hyperpigmentation in hypoadrenalism?
ONLY PRIMARY (addison’s disease). Extra ACTH means extra POMC=extra MSH.
secondary/tertiary hypoadrenalism you don’t see pigmentation.
What type of (hypo/hyper/normo) volemia and natremia does SIADH present with and why?
Euvolemic Hyponatremia.
RAAS system senses fluid overload state and turns off therefore you get dilutional hyponatremia but normal extravascular fluid status (can have very minor hypervoluemia intially, but normalizes rapidly)
Histological Features of the following thyroditsises:
Hypothyroidism dt hashimotos
Papillary Thyroid Cancer
Subacute DeQuervains Thyroiditis
Riedel’s
1) Hashimotos: Mononuclear parenchymal infiltration with well developed germinal centers
2) Papillary: Branching papillary structures with interspersed calcified bodies (+ follicular hyperplasia with tall interfollicular papillary projections)
3) DeQuevarins: Mixed cellular infiltration with occasional multinucleated giant cells.
4) Reidels: Extensive stromal fibrosis that extends beyond the thyroid capsule
Male with foamy urine, comes in with a new left varicocele why?
Patient has nephrotic syndrome and is loosing ATIII thus making blood post glomerulus hypercoagulable. Get a clot in the renal vein which causes back pressure in the spermatic vein
Bilateral Renal Tumors DD?
von Hippel Lindau if they are Renal Cell Carcinoma
TSC if they are angiomyolipomas
First dose HOTN seen with what drug? Particularly if added to which other drug?
ACEI; especially with HCTZ
What type of glomerulus will PSGN show on LM?
Hypercellular Glomerulus
Steroids SEs?
Hypocalcemia, hypokalemia, fluid retention, hyperglycemia, hypernatremia
Renal Cell carcinoma triad?
Hematuria, Abdominal Mass, Flank pain
Pheo’s Effect on BP?
Increased BP but particularly of DIASTOLIC BP (NE/Epi cause Alpha 1 activation leading to increased TPR)
Metyrosine
Inhibits Tyrosine hydroxylase thus inhibits catecholamine synth
Propanolols effects in thyrotoxicosis?
1) Decreased sympathetic outflow to organs
2) Decreased peripheral conversion from T4 to T3***
