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45 Cards in this Set
- Front
- Back
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what would prevent the stones in kidney
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thaizides-- they prevent the stone formation by prevent ca to go in urine, by absorbing Ca
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what could be dangerous for P with renal failuer
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Mg. k and Phosph
may be dangerous and are not prescr for P with RF consult the patient to avoid banana and orange juice( lots of K \ ca is good for kidney- will bindPHospjh and prevent bone loss |
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if patint miss the dialysis what to expect
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metabolic acidosis- with respiratory compen alcalosis
hypokalemia hypomagnesimia |
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common case of renal failure
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dehydration. CHF HTN rhabdom BPH
unilateral nephrolitiasis and 1 kidney would not cause that |
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what are electrolyte picture in P with renal failure
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hyper__ Ph, Mg K
hypo Ca azotemia acidosis also could be pericarditis and decrease imm system , but not auto imm problems |
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large calculi
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could be describe as forning CAST, -- struvite
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alport syndrome
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xlinked, .. abnorm of basement membr of eye , cochlea and glomerula
look for history of deafess hematuria proteiuria progression to end stage -- after childhood |
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posterior urhetral valve
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p[oor dribling urinary stream
may be palpable lower abdmen mass elongation and dilation of posterior urhetra witha prominent bladder neck fopund in distal prostatic urhetra.. tx- valve avlation |
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congenital nephrotic syndrome
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look for scandinavian
placenta megaly is often proteinuria, elevate serum creatinin most kids died at age of 5 |
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IGA nephropatia
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assoc with infection or systemic dieae
hematuria renal casts proteinuria is high but below the range of nephroopaty |
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what is patogn for rapidly progess GN
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creshent formation..
proteniuria renal failure |
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what to give to P after thyroidectomy if Ca is low and why it is low
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accid removal of parathy
giuve thazide-- they are spare CA also give ca gluconate oral ca no PTH- low ca and hight PHosp |
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what is test for renal colic
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CT w/O contrast
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if microhematuria andcyctisis what test
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cystosk
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what to give the P with unilateral a renal artery stemosis
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ACE if HTN
but condition will be correct by surgery |
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if p has nephrotic syndrome , how to confirn
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24 urine protein
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membranous glomerulonephritis
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edema
weight gain thick glom nephr loop 40 % of adult nephrotic syndromes |
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iga nephropathy
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look for respir infection immediately- hemarturia with or w/o proteinuria
GN after poststrep- will be in 2 weeks!! this is difference!! also may be in young people after vigorous exers renal biopsy- mesangial proliferation and glomerula IgA deposition |
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muddy browm cast .. when?
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acute tubiular necrosis
they dont change the color of urine but coud be seen on microscopy |
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HUS
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microangiopatic hemol anemia\ trombocytopenia
acute renal failure HMc low platelets low BUN, Cr- high |
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protein- creatinin ration with range 1.0-- mean
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nephrotic range of proteiuria
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apin hematuria abdom mass weight loss
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90 solid tumors are renal carcinoma
thwy connect to Hippel lindau and 3 chrom |
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renal adenocarcinoma
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related to smoking
men>women 60-70- yeas affect poles of kidney hematuria pain( clot formation) secrete erytropoetin ( secondary polycythemia) parathhormone like peptide-- >>> hypercalcemia renin...>> HTN gonadotrthropn>>. feminisation or maskulinization can- nonball mts ... in lungs up to 60% |
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A 45-year-old diabetic with a foot ulcer and gram-negative septicemia is being treated with IV gentamicin therapy for the past 7 days. A routine laboratory study done 2 days ago showed a serum potassium of 2.8 mEq/L. Despite potassium supplementation in IV fluids at 40 mEq/L, for the past 2 days the serum potassium today is still 2.7 mEq/L.
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Aminoglycoside therapy is associated with hypokalemia and also hypomagnesemia. When the magnesium levels are low, it makes hypokalemia resistant to therapy unless magnesium deficiency is corrected
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HypomagnesemiaSYMPTOMS AND SIGNS
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Hypomagnesemia
SYMPTOMS AND SIGNS Hypomagnesemia is very common but, as with hypophosphatemia, is often overlooked or ignored. Magnesium is essential for a broad range of biologic processes, and thus hypomagnesemia may cause a broad array of systemic abnormalities ). It may cause hypocalcemia, seizures, and paresthesias independent of hypocalcemia, and may cause a broad array of neuromuscular, cardiovascular, or respiratory symptoms. Commonly, this occurs in an ICU setting in which magnesium administration and diet are inadequate, magnesuric intravenous saline is administered along with diuretics, and serum magnesium is never measured. It responds rapidly and dramatically to parenteral magnesium replacement. |
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2 way of Mg loss
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Inadequate Intake
Inadequate intake of magnesium is common among alcoholics and the generally undernourished. It may occur as part of an intestinal malabsorption syndrome, and may result from continuous vomiting or nasogastric suctioning. Again, these are all common in ICU settings, and are often overlooked. Excessive Renal Losses Excessive renal losses of magnesium are also common in clinical practice; thiazide and loop diuretics both cause renal magnesium losses, and saline infusion has a similar effect. Magnesium is also lost by the kidney in response to aldosterone in primary hyperaldosteronism, but more commonly in the secondary hyperaldosteronism associated with cirrhosis, volume depletion, congestive heart failure, and other common disorders. Osmotic diuresis, as occurs, for example, with poorly controlled diabetes mellitus, causes renal magnesium loss. Certain nephrotoxic drugs such as cisplatin, aminoglycoside antibiotics, and amphotericin induce proximal tubular injury and a severe form of renal magnesium wasting. Hypokalemia may lead to magnesium wasting by the kidney, and the reverse is true as well. Hypercalcemia and hypercalciuria lead to renal magnesium excretion as well, although the cellular basis for this is not fully understood. Finally, many diseases that lead to proximal tubular injury, such as Fanconi's syndrome and interstitial nephritis, may lead to magnesium wasting. |
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High BUN and serum uric acid levels suggest hypovolemia
When hyponatremia is associated with a low BUN and uric acid level, what is the most likely diagnosis. |
When hyponatremia is associated with a low BUN and uric acid level, SIADH is the most likely diagnosis.
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36-year-old woman with hypertension is being treated with an ACE inhibitor, a beta blocker, and aldosterone receptor blocker. All the three medications are very well known to cause ....
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36-year-old woman with hypertension is being treated with an ACE inhibitor, a beta blocker, and aldosterone receptor blocker. All the three medications are very well known to cause hyperkalemia. Therefore, a patient receiving all three drugs is at a high risk of developing hyperkalemia.
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k approach
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what is the major determinant of the resting potential of the cell membrane
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The ratio of intracellular to extracellular potassium concentration is the major determinant of the resting potential of the cell membrane. As the extracellular potassium concentration increases, the cell membrane is partially depolarized, the sodium permeability is diminished, and the ability to generate action potentials is decreased. In muscle tissue, this change accounts for muscle weakness and paralysis. In the heart, hyperkalemia is manifested as changes in the electrocardiogram. These changes include peaked T waves, decreased amplitude or the absence of P waves, wide QRS complexes, sinus bradycardia, and conduction defects.
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Normal values of urine gravity is
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Normal values are between 1.020 to 1.028.
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Increased urine specific gravity may be due to:
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Increased urine specific gravity may be due to:
Addison's disease (rare) Dehydration Diarrhea that causes dehydration Glucosuria Heart failure (related to decreased blood flow to the kidneys) Renal arterial stenosis Shock Syndrome of inappropriate antidiuretic hormone secretion (SIADH) |
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Decreased urine specific gravity may be due to:
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Decreased urine specific gravity may be due to:
Aldosteronism (very rare) Excessive fluid intake Diabetes insipidus - central Diabetes insipidus - nephrogenic Renal failure Renal tubular necrosis Severe kidney infection (pyelonephritis) |
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Higher than normal levels of osmolalty may indicate:
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Higher than normal levels may indicate:
Dehydration Diabetes insipidus Ethylene glycol poisoning Hyperglycemia Hypernatremia Methanol poisoning Renal tubular necrosis Stroke or head trauma resulting in deficient ADH secretion Uremia |
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lower than normal levels of osmolalty may indicate:
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Excess fluid intake
Hyponatremia Overhydration Paraneoplastic syndromes associated with lung cancer Syndrome of inappropriate ADH secretion |
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Gonococcal urethritis and cervicitis:
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Gonococcal urethritis and cervicitis: Treatment should be directed against Chlamydia trachomatis as well as N. gonorrhoeae because dual infection is common.
Anti-gonococcal drugs include cefixime, ceftriaxone, azithromycin, and quinolones (ciprofloxacin or ofloxacin). Anti-chlamydial drugs include tetracycline, doxycycline, ofloxacin, and azithromycin. |
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classic simple virilizing form of congenital adrenal hyperplasia
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classic simple virilizing form of congenital adrenal hyperplasia, an autosomal recessive disorder of adrenal corticosteroid biosynthesis. The most common type is 21-hydroxylase deficiency which results in excess adrenal androgen production in utero and subsequent genital virilization in genetic females.
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5-Alpha-reductase deficiency
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5-Alpha-reductase deficiency is an autosomal recessive condition characterized by the inability to convert testosterone to dihydrotestosterone. Phenotypic findings in a newborn range from micropenis or hypospadias to severe undervirilization presenting as normal female external genitalia.
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Addison diseas
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Addison disease usually presents with hyperpigmentation of the skin and mucous membranes, dehydration, and hypotension, not virilization.
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congenital adrenal hypoplasia may present with
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Although congenital adrenal hypoplasia may present with hyperpigmentation from increased adrenocortictropic, it is most commonly diagnosed in the neonatal period with dehydration, hyponatremia, hyperkalemia, hypotension, or hypoglycemia.
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Androgen insensitivity syndrome (AIS) is
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Androgen insensitivity syndrome (AIS) is an X-linked recessive condition resulting in a failure of normal masculinization of the external genitalia in chromosomally male individuals. Most cases of AIS are identified in the newborn period by the presence of inguinal masses, which later are identified as testes during surgery.
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The most important problem caused by accumulation of steroid precursors is
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The most important problem caused by accumulation of steroid precursors is that 17-hydroxyprogesterone is shunted into the pathway for androgen biosynthesis, leading to high levels of androstenedione that are converted outside the adrenal gland to testosterone. This problem begins in affected fetuses by 8-10 wk of gestation and leads to abnormal genital development in females
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The external genitalia of males and females normally appear identical early in gestation (see Chapter 576). In normal females, the genital tubercle becomes
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The external genitalia of males and females normally appear identical early in gestation (see Chapter 576). In normal females, the genital tubercle becomes the clitoris; the urethral folds develop into the labia minora, and the labioscrotal swellings become the labia majora.
In males, development of the external genitalia is normally controlled by testosterone secreted by the fetal testes. The genital tubercle enlarges to become the glans of the penis; the urethral folds fuse to form the shaft of the penis and penile urethra, and the labioscrotal swellings fuse to form the scrotum. |
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Testosterone
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Testosterone also controls the development of the wolffian ducts into male internal genital structures such as the prostate, spermatic ducts, and epididymis, but higher levels of testosterone are required than for development of the male external genitalia. In contrast, testosterone has no effect on development of female internal reproductive structures (cervix, uterus, and fallopian tubes) from müllerian ducts. In male fetuses, these structures involute under the influence of anti-müllerian hormone (müllerian inhibitory factor) secreted by the testes.
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affected females, who are exposed in utero to high levels of androgens of adrenal origin, have
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affected females, who are exposed in utero to high levels of androgens of adrenal origin, have masculinized external genitalia. This is manifested by enlargement of the clitoris and by partial or complete labial fusion. The vagina usually has a common opening with the urethra (urogenital sinus). The clitoris may be so enlarged that it resembles a penis and, because the urethra opens below this organ, some affected females may be mistakenly presumed to be males with hypospadias and cryptorchidism. The severity of virilization is greatest in females with the salt-losing form of 21-hydroxylase deficiency. The internal genital organs are normal, because affected females have normal ovaries and not testes and thus do not secrete anti- müllerian hormone.
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