Deck 2 Flashcards
What are the 3 layers of the adrenal gland?
GFR
Glomerulosa: Aldosterone controls Na balance (outer layer)
Fasciulata: Cortisol (middle layer)
Reticularis: produces androgen/estrogen (inner layer)
Cushing’s Syndrome:
S/s related to cortisol excess
Cushing’s disease:
cushing’s syndrome caused specifically by pituitary incr ACTH secretion
What are EXOGENOUS causes of Cushing’s syndrome
Iatrogenic - long term high dose corticosteroid use
What are ENDOGENOUS causes of Cushing’s syndrome
Cushing's Disease (70%) Ectopic ACTH (15%) Adrenal Tumor (15%)
What is the lung cancer that is an endogenous cause of cushing’s syndrome
Small Cell Lung Cancer secreting ACTH
What are the Clinical Presentations of Cushing’s Syndrome:
- Redistribution of Fat
- central obesity
- moon facies
- buffalo hump
- supraclavicular fat pads - catabolism of protein
- wasting (thin) of extremities
- prox muscle weakness
- increased infections
- skin atrophy
- hyperpigmentation - Hypertension
- Androgen excess (hirsutism)
How do you diagnose Cushing’s syndrome?
- Low-dose dexamethasone suppression test
- Incr 24hr urinary free cortisol levels
- Incr salivary cortisol levels
What would you expect CMP lab results to be if a patient is in Addison’s crisis?
HYPOnatremic
HYPOglycemic
HYPERkalemic
HYPERcalcemic
How do you treat someone in Addison’s crisis:
- IV normal saline for Hypovolemia (D5NS if hypoglycemic)
- Replenish Sodium
- Give K-exylate to decrease potassium
- Florinef (to replace aldosteron)
- if known addisons = hydrocortisone
- if undiagnosed = dexamethasone
At what serum glucose level, does glucose start spilling into the urine?
180mg/dL.
-normally the kidney reabsorbs nearly all glucose, the renal threshold for glucose is 180mg/dL.
Where in the kidney (nephron) does Acetazolamide work?
-the proximal tuble
What is the primary function of the proximal tubule?
-reabsorption of vital substances
Where does Mannitol work in the nephron?
-proximal tuble
What substances are reabsorbed in the proximal convoluted tubule?
- 75% Na
- glucose
- Amino acids
- most bicarbonate (HCO3)
- Chloride
- 75-90% of H2O
The Thick Ascending Limb (TAL) of Loop of Henle is IMPERMEABLE to H20, but absorbs what substances?
Actively reabsorbs: Na+, K+, & Cl-
Indirectly reabsorbs Mg+ & Ca+
Where do diuretics like furosemide, bumetanide, ethacrynic acid, & torsemide work in the kidney?
Furosemide, Bumetanide, Ethacrynic acid, and torsemide are all examples of Loop Diuretics.
Loop Diuretics work in the Thick Ascending Limb of the Loop of Henle.
What is the MOA for Loop Diuretics?
They work on the Thick Ascending Limb, to inhibit the reabsorption of solutes.
When Na+, Cl-, K+, Mg+ and Ca+ are not reabsobed, a person becomes:
Hyponatremic
Hypochloremic > incr. biocarb reabsorption >met. alkalosis
Hypokalemic
Hypocalcemic
Hypomagnesemic
Concentrated urine means:
1. physiologically what is happening? 2. resulting in a solute to H2O ratio? 3. High or low specific gravity?
Something is happening in the kidneys causing solutes (Na, K, Cl, Ca, Mg, glucose) to not be reabsorbed into the body…thus causing increased amounts being excreted through the urine & decreased amount in the blood.
more solute > H2O ratio.
concentrated urine = high specific gravity
What does Dilute Urine mean?
- What is happening physiologically?
- what is the solute to H2O ratio?
When urine is more dilute it means there is a physiologic process occurring in the kidneys increasing the amount of solutes (Na, K, Cl, Ca, Mg, glucose) that are being reabsobed.
Where do chlorothiazide, chlorthalidone, HCTZ, indapamide, methyclothiazide, and metolazone work in the kidney?
chlorothiazide chlorthalidone HCTZ indapamide methyclothiazide metolazone are all examples of Thiazide Diuretics they work on: the cortical-diluting segment of the ascending loop of Henle
What is the MOA of Thiazide Diuretics?
inhibits sodium and chloride reabsorption in the cortical-diluting segment of the ascending loop of Henle
Where does Angiotensin II act on the kidneys?
What does it cause?
Proximal Tubules
Causing Incr. Na & H2O reabsorption.
Where does Aldosterone work in the Kidneys?
What does it do?
Collecting Duct, (Distal)!
Incr. reabsorption of Na+ in exchange for decr. reabsorption of K+ & H+
Hyperaldosteronism is commonly associated with what electrolyte disorder(s)?
Hypokalemia
Metabolic alkalosis
because K+ and H+ are being excreted through the urine, so Na is spared.
Where does Spironolactone work in the kidney?
the distal collecting ducts of the renal tubules.
What is the MOA for potassium-sparing diuretics?
Competes with aldosterone for receptor sites in the distal renal tubules –>
less aldosterone ->
decr. reabsorption of Na+, Cl-, H2O –>
Incr. Na+, Cl-, & H2O excretion,
while conserving potassium and hydrogen ions; may block the effect of aldosterone on arteriolar smooth muscle as well
What are common SE of Spironolactone?
HYPERkalemia & Metabolic Acidosis
Hyponatremia, Hypochloremia
Vasopressin is an example of what class of medication?
Antidiuretic Hormone.
What is the MOA of Vasopressin?
Vasopressin stimulates a family of arginine vasopressin (AVP) receptors, oxytocin receptors, and purinergic receptors (Russell 2011). Vasopressin, at therapeutic doses used for vasodilatory shock, stimulates the AVPR1a (or V1) receptor and increases systemic vascular resistance and mean arterial blood pressure; in response to these effects, a decrease in heart rate and cardiac output may be seen. When the AVPR2 (or V2) receptor is stimulated, cyclic adenosine monophosphate (cAMP) increases which in turn increases water permeability at the renal tubule resulting in decreased urine volume and increased osmolality. Vasopressin, at pressor doses, also causes smooth muscle contraction in the GI tract by stimulating muscular V1 receptors and release of prolactin and ACTH via AVPR1b (or V3) receptors.
What are nephrotoxic causes of Acute Tubular Necrosis?
Exogenous:
- Aminoglycosides (amikacin, gentamicin, streptomycin, tobramycin).
- contrast dye
- Cyclosporine
Endogenous:
- gout (crystal precipitation),
- myoglobin (rhabdomyolysis)
- lymphoma
- leukemia
- Bence Jones (multiple myeloma)
What is common findings of Acute Tubular Necrosis cause of intrinsic AKI?
Muddy brown casts on UA because of tubular damage, epithelial casts, waxy/grannular casts.
What are common Medications that can cause Acute interstitial Nephritis (AIN)?
Penicillins NSAIDs Sulfa drugs cephalosporins ciprofloxacin rifampin allopurinol
What is a PATHOGNOMIC finding on UA for AIN?
WBC casts
Urine Eosinophils
Urinalysis results:
RBC Casts
Hematuria
Dysmorphic Red cells
Acute Glomerulonephritis or Vasculitis
Also expect to see: Urine Spec gravity 1.010 - 1.020 & BUN:Cr ratio <15:1
Patient is in Acute Kidney Injury with Intrinsic cause
Urinalysis results:
Granular (muddy brown) casts
+/- epithelial cell casts
Acute Tubular Necrosis
UA results with:
WBC casts
pyuria
Acute Interstitial Nephritis (AIN) or Pyelonephritis or tubular disease
UA with narrow waxy casts
Chronic - Acute Tubular Necrosis or Glomerulonephritis
UA with Broad waxy casts
END STAGE RENAL DISEASE (tubal dilation)
UA with Fatty casts or maltese crosses, oval fat bodies
Nephrotic Syndrome (d/t hyperlipidemia)
Hyaline casts
non-specific & may be normal
Hematuria & pyuria without red cell casts
UTI
Acute interstitial Nephritis
Glomerular disease
vasculitis
GFR of 60 - 89 is:
Stage 2 CKD
GFR >90 in presence of proteinuria, abnormal UA, serum or imagining kidney damage
Stage 1 CKD
GFR 30 to 44 is
Stage 3b CKD
GFR of 45 to 59 is
Stage 3a CKD
GFR <15 is
ESRD = uremia requiring dialysis and/or transplant
GFR 15-29 is
Stage 4
