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Renal II Flashcards

1
Q

Type II RTA

A

Defect in bicarbonate reabsorption

Faconi, PAGU

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2
Q

Isolated proximal RTA

A

Hereditary dysfunction of basolateral sodium bicarbonate cotransporter

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3
Q

What causes faconi

A

Inherited or acquired due to myeloma, chronic IN (Chinese herbal nephropathy), or drugs (ifosfamide, tenofovir)

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4
Q

Treat type II or faconi

A

Large doses of bicarbonate which may aggravate hypokalemia

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5
Q

Type IV

A

Hyporeninemic hypoaldosteronism or resistance

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6
Q

50-80% of women have at least one __ and 20-50% have recurrent episodes

A

UTI

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7
Q

Ribs factors for acute cystitis

A

Recent use of diaphragm with spermicide, frequent sexual intercourse, a history of UTI, DM, incontinence; also increase risk of pyelonephritis

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8
Q

Most common UTI bacteria

A

E. coli 75-90

Staph saprophyticus 1-15%

Klebsiella , proteus, enterococcus, citrobacter rest

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9
Q

Iwhat gram positives cause UTI

A

Staph aureus and enterococci

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10
Q

Candida UTI path different than other organisms

A

Hematogenous route

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11
Q

Candida in urine or noninstrumetned immunocompetent

A

Genital contamination or widespread visceral dissemination

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12
Q

Papillary necrosis

A

Can occur in pets with obstruction, dibatetes, sickle cell disease, or analgesic nephropathy

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13
Q

Emphysematous pyelonephritis

A

Severe

Associated with the production of gas in renal and perinephric tissues, and occurs almost exclusively in diabetics

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14
Q

Xanthogranulomatous pyelonephritis

A

Chronic urinary obstruction (often staghorn), together with chronic infection, leads to suppurative destruction of renal tissue

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15
Q

Prostatis

A

Infectious or not

More common not

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16
Q

Complicated UTI

A

Symptomatic disease in a man or woman with an anatomical predisposition to infection, with a foreign body into e urinary tract, or with factors predisposing to a delayed response therapy

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17
Q

Diagnose UTI uncomplicated

A

Clinical history 96% LIEKLYHOO if have dysuria and urinary frequency in absence of vaginal discharge

Confirm with dipstick positive for nitrite or leukocyte esterase in patients with a high pretext probability of disease

Detection of bacteria in a urine culture is gold standard
Want colon count 10^2 OR OVER

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18
Q

What three factors determine the initial rate of spread of any STI within a population

A

Rate of sexual exposure of susceptible to infectious ppl, efficiency of transmission per exposure, and duration of infectivity of those infected

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19
Q

What are 4C’s of sti

A

Contact tracing, ensuring compliance with treatment, counseling on risk education, including condom promotion and provision

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20
Q

What causes urethritis in men

A

Gonococcal or nongonococcal (chlamydia trachomatis)

Mycoplasma genitalium, ureaplasma, urealyticum, trichomonas vaginalic, HSV

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21
Q

What causes most non gonococcal urethritis in men

A

Chlamydia and mycoplasma genitalium

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22
Q

Symptoms or male urethritis

A

Urethral discharge, dysuria, without frequency of urination

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23
Q

Diagnose male urethritis

A

Pts present with mucopurulent urethral discharge can be expressed by milking the urethra

Grams stained smear of an anterior urethral specimen containing 5PMN/1000x field confirms the diagnosis

Centrifuged sediment of the days first 20-30 mL or voided urine can be examined instead

N gonorrhea can be identified if intracellular gram negative diplodocus are present in grams strained samples

Early oring, first voided uring should be used in multiplex acid amplification testes (NAATs ) for gonorrhea and chlamydia

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24
Q

Treat gonorrhea

A

Ceftriaxone

Azithromycin

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25
Q

Treat chlamydia

A

Azithromycin

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26
Q

Treat mycoplasma genitalium

A

Azithromycin

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27
Q

Treat recurrent symptoms of male urethritis

A

Both patient and partner treated if re exposure

Without re exposure, infection with T vaginalis (with culture or NAATs)

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28
Q

Shock

A

Ok

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29
Q

Possibly harmful systemic response to shock

A

Two or more of the following

  • fever or hypothermia
  • tachypnea
  • tachycardia
  • leukocytosis
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30
Q

Sepsis

A

Harmful systemic response with a proven or suspected microbial etiology

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31
Q

Septic shock

A

Sepsis with hypotension (90< or below pts normal bp for at least 1 h despite fluid resuscitation) or need for vasopresors to maintain systolic bp 290 mmHg or MAP 270 mmHg

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32
Q

Etiology shock

A

Blood cultures are positive in 20-40% of sepsis causes and in 40-70% of septic shock cases

For infected patients in ICUs, respiratory infections have been most common (64%) . Microbiological results have revealed that 62% of isolates are gram negative bacteria (pseudomonas spp and E. coli) , 47% are gram positive (staph aureus) and 19% are fungi (candida)

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33
Q

Epidemiology shock

A

Incidence of severe sepsis and septic shock in US increases with >750000 cases each year contributing to over 200000 deaths. Invasive bacterial infections are a prominent cause of death areound the world, especially among young kids

Sepsis related incidence and mortality rates increases with age and preexisting comorbidity, with 2/3 of cases occurring in pts with significant underlying disease

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34
Q

What has the increased incidence of sepsis been attributed to

A

The aging population, longer survival of patients with chronic disease, a relatively high frequency of sepsis among AIDS, and medical treatments that circumvent host defenses 9immunosuppresive agents, catheters)

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35
Q

Local and systemic host response to septic shock

A

Hosts have numerous receptors that recognize highly conserved microbial molecules, triggering the release of cytokines and other host molecules that increase blood flow and neutrophil migration to the infected site, enhance local vascular permeability, and elicit pain

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36
Q

Many local and systemic control mechanisms for septic shock dismiss cellular responses to what

A

Microbial molecules,
-intravascular thrombosis (which prevents spread of infection and inflammation) and an increase in anti inflammatory cytokines (IL4 and 10(

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37
Q

Organ dysfunction and shock

A

Widespread vascular endothelial injury is believed to be the major mechanism for multiorgan dysfunction
Septic shock is characterized by compromised oxygen delivery to tissues followed by a vasodilary phase ( a decrease in peripheral vascular resistance despite increased levels of vasopressin catecholamines)

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38
Q

Clinical features septic shock

A

Hyperventilaition that produces respitoary alkalosis

Encephalopathy (disorientation, confusion)

Acrocyanosis and ischemic necrosis of peripheral tissues due to hypotension and DIC

Skin-hemorrhagic lesions, bullae, cellulitis, pustules. Skin lesions may suggest specific pathogens

GI-nausea, vomiting, diarrhea, ileus, cholestatic jaundice

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39
Q

What infection suggested petechiae and purpura

A

Neisseria meningitidis

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40
Q

What skin infection ssuggests pseudomonas aeruginosa

A

Acthyma and gangrene

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41
Q

Cardiopulmonary manifestations of septic shock

A

Ventilation-perfusion mismatch, increased alveolar capillary permeability, increased pulmonary water content, and decreased pulmonary compliance impede oxygen exchange and lead to ARDS (progressive diffuse pulmonary infiltrates and arterial hypoxemia) in 50% of patients

Hypotension: normal or increased cardiac output and decreased systemic vascular resistance distinguish septic shock from cardiogenic and hypovolemia shock

The ejection fracture is decreased, but ventricular dilation allows maintence of a normal stroke volume

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42
Q

Adrenal insuffiency of septic shock

A

May be difficult to diagnose in critically ill patients

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43
Q

Renal manifestations septic shock

A

Oliguria and polyuria, azotemia, proteinuria and renal failure due to tubular necrosis

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44
Q

Neurological manifestations of septic shock

A

Delirium in the acute phase, polyneuropathy with distal motor weakness in prolonged sepsis. Survivors may have long term cognitive impaiement

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45
Q

Immunosuppression with septic shock

A

Patients may ave reactivation of HSY, CMV, or VZv

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46
Q

CBC SEPTIC SHOCK

A

LEUKOCYTOSIS WITH A LEFT SHIFT, thrombocytopenia

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47
Q

Coagulation with septic shock

A

Prolonged thrombin time, decreased fibrinogen, presence of n diners suggestive of DIC. With DIC , platelet counts usually fall below 50000

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48
Q

Chemistries septic shock

A

Metabolic acidosis, elevated anion gap, elevated lactate levels

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49
Q

LFTs septic shock

A

Transaminitis, hyperbilirubinemia, azotemia

Hypobilirubinemia

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50
Q

Diagnose septic shock

A

Need isolation of microorganisms from blood or a local site of infection. Culture of infected cutaneous lesions may help establish the diagnosis

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51
Q

Treat septic shock and sepsis

A

Antibiotic

Removal of drainage of a focal source of infection

Hemodynamics, respiratory, and metabolic support
-saline, hydrocortisone(if hypotension not responding), erythrocytes transfusion

General support

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52
Q

Prognosis septic shock

A

20-35% of patients with severe sepsis and 40-60% of patients with septic shock die within 30 days , and further deaths occur within 6 months. Prognostic stratification systems can estimate the risk of dying of severe sepsis

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53
Q

Oliguria

A

Less than 400

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54
Q

Anuria

A

No Rhine

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55
Q

Setting of oliguria

A

Volume depletion and/or renal hypoperfusion, resulting in prerenal azotemia and acute renal failure

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56
Q

What can cause anuria

A

Complete bilateral urinary tract obstruction; a vascular catastrophe, renal vein thrombosis; renal cortical necrosis; severe acute tubular necrosis; nonsteroidal antiinflammatory drugs, ACE I, angiotensin receptor blockers , hypovolemia, cardiogenic or septic shock

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57
Q

Polyuria

A

Over 3 Lid

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58
Q

Setting of polyuria

A

Nocturnal and urinary frequency , hypernatremia and can occur as a response to solute load and vasopressin ADH

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59
Q

Diabetes insipidus

A

Central insufficient AVP

Nephrogenic-insensitivity

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60
Q

What is associated with nephrogenic diabetes insipidus

A

Tubulointerstitial diseases, lithium therapy, and resolving acute tubular necrosis or urinary tract obstruction can be associated with nephrogenic diabetes insipidus, which is more rarely caused by mutations in the V2 AVP receptor, the aquaporin 1 water channel in the descending thin limb of the loop of henle and the AVP regulated water channel in principal cells, aquaporin 2

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61
Q

Proteinuria causes

A

Excessive fluid intake-primary polydipsia, latrogenic (IV)

Therapeutic-diuretics

Osmotic diuresis-hyperglycemia

Azotemia
Mannitol

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62
Q

Nephrogenic diabetes insipidus cause

A

Lithium, UT obstruction, papillary necrosis, reflux nephropathy, interstitial nephritis, hypercalcemia, hereditary

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63
Q

Causes central diabetes insipidus

A

Tumor, postoperative, head trauma, basilar meningitis, neurosarcoidosis

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64
Q

Polyuria with <250 mosmol and low serum sodium

A

Primary polydipsia

=psychogenic, hypothalamic disease drugs(thioridazine, chlorpromazine, anticholinergic agents)

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65
Q

Polyuria urine osmolarity <250 and diabetes insipidus

A

Nephrogenic DI vasopressin

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66
Q

Polyuria urine osmolarity >300

A

Solute diuresis

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67
Q

Diagnose proteinuria

A

Dipstick estimates protein concentration

Detect albumin, not light chains (require testing with sulfosalicylic acid)

Urine albumin

24 hour protein collection

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68
Q

When may transient proteinuria be seen

A

After vigorous exercise, changes in body position, fever, or CHF

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69
Q

What is nephrotic range proteinuria

A

3 g/d

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70
Q

When can massive proteinuria be seen

A

MCD, primary focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy, collapsing glomerulopathy

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71
Q

How treat proteinuria

A

ACE inhibitor or angII blocker

This will decrease rate of progression to end stage renal disease in diabetic nephropathy

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72
Q

Hematuria causes

A

Lower urinary tract disease or intrinsic renal disease

Cyst rupture in polycystic kidney disease and postpharyngitic flares of IgA nephropathy

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73
Q

Microscopic hematuria accompanies by proteinuria, HTN, and an active urinary sediment is most likely related to an inflammatory glomerulonephritis, classically post streptococcal glomerulonephritis

A

Ok

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74
Q

Major causes of hematuria lower urinary tract

A 
Bacterial cystitis
Interstitial cystitis
Urethritis
Passes or passing kidney stone
Transitional cell carcinoma of bladder or structures proximal to it
Squamous cell carcinoma of bladder
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75
Q

Upper urinary tract causes of hematuria

A

Renal cell arcinoma

Age related renal cysts

Neoplasms
Acquired renal cystic disease
Congenital cystic disease, including autosomal dominant form
Glomerular diseases
Intestinal renal diseases)interstitial nephritis

Nephrolithiasis, pyelonephritis
Renal infarction, hypercalcuria, hyperuricosuria

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76
Q

Free hemoglobin and myoglobin on dipstick and negative urinary sediment with strong heme positive dipstick

A

Hemolysis or rhabdomyolysis, which can be differentiated by clinical history and laboratory testing

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77
Q

RBC cast specific for what

A

Glomerulonephritis

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78
Q

Acute renal failure/ AKI

A

Measurable increase in serum Cr concentration and happens in 5% of hospitalized patients and associated with increase in hostpital mortality and morbidity

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79
Q

Treat AKI

A

Nothing specific maintain renal perfusion and intravascular volume

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80
Q

Cofactors of AKI

A

Hypovolemia and drugs that interfere with renal perfusion and/or glomerular filtration (NSAIDS) ACE I ang blockers

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81
Q

Prerenal failure

A

Most common in hospital
May result from true volume depletion or arterial underfilling (reduced renal perfusion in the setting of adequate or excess blood volume

Reduced renal perfusion may be seen in CHF

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82
Q

Pre renal causes of AKI

A

Volume depletion-blood loss, diuretic use

Volume overload with reduced renal perfusion-CHF, hepatic cirrhosis, severe hypoporteinemia

Renovascular disease

Drugs-NSAIDS, ciclosporin,

Hypercalcemia “third spacing )pancreatitis, systemic nflammatory response, whepatorenal syndrome

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83
Q

Intrinsic causes of AKI

A

ATN

Ttubulointerstitial diseaseatheroembolic disease after vascular procedures

Glomerulonephritis

IgA nephropathy

Glomerular endoliopathies

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84
Q

Post renal AKI

A

Bladder neck obstruction, bladder calculi

Prostatic hypertrophy, urethral obstruction due to compression
-pelvic or ab malignancy

Nephrolithiasis

Papillary necrosis with obstruction

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85
Q

Causes of intrinsic failure in hspoiratl

A

Surgical services or ICU, ATN, rhabdomyolyssi, allergic penicillins, NSAIDS, radiographically contrast dies, thrombotic microangiopathies,

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86
Q

Post renal

A

Ambulatory more common than hospitalized more common men

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87
Q

AKI with prerenal azotemia due to volume depletion presentation

A

Orthostatic hypotension, tachycardia, low jugular venous reassure, anddry mucoud membranes

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88
Q

Prerenal azotemia and CHF

A

Jugular venous distention and S gallop, peripheral and pulmonary edema.

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89
Q

Signs pre renal

A

BUN Cr high, volume depletion and CHF cirrhosis

Uric acid may be up

Na <10-20 urine FEN <1%

Hyaline and few granular casts, without cells or cellular casts . Renal ultrasonography is usually normal

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90
Q

Intrinsic renal disease GN

A

HTN and edema

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91
Q

Fractional excretion of Na

Urine Na

Urine Cr to plasma ratio

Urine urea N to plasma uraea N
Urine specific gravity

Urine osmolality
Plasma BUN/Cr ration

Renal failure index

Urnary sediment

Prerenal vs intrinsic

A

<1, >1
<10, >20

> 40, >20

> 8, <3

> 1.018, <1.015

> 500, <300

> 20, <10-15

<1, >1

Hyaline casts, muddy brown granular casts

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92
Q

Dialysis

A

ESRD-depends on patients symptoms, comorbid conditions and laboratory parameters, unless a living donor is identified, transplantation is deferred by necessity, due to the scarcity of decreased donor organs . Dialysis options include hemodialysis and peritoneal dialysis. Roughly 85% of US patients are started on hemodialysis. Absolute indications for dialysis include severe volume overload refractory to diuretic agents, severe hyperkalemia and/or acidosis, severe encephalopathy not. Otherwise explained, and pericarditis or other serositis. Additional indications for dialysis include symptomatic uremia, nause, vomiting , pruritis, difficulty maintains attention and concentration. And protein every malnutrition failure to thrive without other overt cause.

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93
Q

Complications of hemodialysis

A 
Hypotension 
Accelerated vascular disease
Rapid loss of residual renal function
Access thrombosis
Access or Cather sepsis

Dialysis related amyloidosis
Protein energy malnutrition
Hemorrhage
Anaphylactic reaction

Thrombocytopeniab

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94
Q

Hemodialysis

A

Direct access to the circulation, either via a native arteriovenous fistula; an arteriovenous graft, usually make of polytetra fluoriethylele; a large bore IV catherter , or a subcutaneous device

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95
Q

Solution in dialysis

A

Isotonic, free of urea and other nitrogenous compounds and generally low in K a

Dialysate (K) is varied from 1 to 4 , depending on predialysis K and clinical setting
Ca is typically and Na can be modified , depending on clinical

Usually 3 times a week for 3-4 hours

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96
Q

Peritoneal dialysis

A

Peritoneal catheter allows infusion of a dialysate solution into the abdominal cavity; this allows transfer of solutes across the peritoneal membrane, which serves as the artificial kidney, this solution is similar to that used for hemodialysis, except that is must be sterile

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97
Q

LO

A

Differentiate between uncomplicated UTI and complicated

Develop a differential diagnosis for dysuria based on pre disposing factors, clinical presentation, history and physical

Distinguish cystitis from pyelonephritis and their predisposing factors

Compare and contrast pyelonephritis with sepsis

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98
Q

35 male with dysuria for three days, urine is cloudy and yellow

There is drainage noted from end of penis

Multiple female partners with occasional condom use

A

Ok

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99
Q

Frequency

A

Every hour or two

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100
Q

Urgency

A

Abrupt strong and overwhelming

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101
Q

How frond ABU

A

Urine sample is obtained for another reason and shows bacteria on microscopic evaluation , like health screening or diabetes follow up

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102
Q

What is an uncomplicated UTI

A

Non pregnant female

No anatomical abnormalities

No instrumentation or urinary tract

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103
Q

Predisposing factors for female UTI

A

Use of spermicide with diaphragm

Frequent sex

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104
Q

What percent of women have recurrent UIT

A

20-30%

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105
Q

Recurrent of UTI in post menopausal females predisposing factors

A

Pre menopausal UTI

Anatomic factors affecting bladder emptying

  • cystocele
  • urinary incontinence
  • residual urine
  • tissue effect of estrogen depletion
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106
Q

Predisposing factors for male UTI

A

Prostatic hypertrophy

Non circumcised

Diabetic

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107
Q

Diabetic women are _x more likely to get UIT

A

2-3

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108
Q

Differential diagnosis for UTI

A

Cystitis

Cervicitis

  • chlamydia
  • neisseria

Vaginitis

  • candida
  • trichomonas

Urethritis-herpetic

Interstitial cystitis

Non infectious vaginal or vulvar irritation

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109
Q

Complicated UTI

A

Pregnant female-can lead to premature labor or low birth weight babies

More likely to develop sepsis

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110
Q

Untreated asymptomatic bacteriuria is more likely to cause what in pregnant women

A

Symptomatic pyelonephritis

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111
Q

Causes of complicated UTI in men and women

A

Anatomic variant (polycystic kidney

Foreign body in the urinary tract
-stones, urinary catheters, nephrostomy tubes/ureteral stents

Extrinsic compression of ureter/bladder

  • tumors
  • profound constipation
  • other anomalies

Immune suppression conditions

  • diabetes
  • drugs induced
  • HIV/AIDS
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112
Q

Prostatis

A

Can be chronic in prostatic hypertrophy

Prolonged antibiotic course necessary for 4-6 weeks

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113
Q

Most common precursors of pyelonephritis

A

Same as UTI
-since most commonly ascending from lower tract

Bacteremia develops in 20-30% of cases

Can be hematogenous but rare

  • candida
  • salmonella
  • staph aureus
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114
Q

Three major subtypes/complications of pyelonephritis

A

Papillary necrosis

Emphysematous pyelonephritis

Xanthogranulomatous pyelonephritis

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115
Q

When does papillary necrosis occur

A

Obstruction

Diabetes

Sickle cell

Analgesic nephropathy

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116
Q

Emphysematous pyelonephritis

A

Production of gas in nephrin and perinephric area

Occurs almost exclusively in diabetic patients

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117
Q

Xanthogranulomatous pyelonephritis

A

Chronic obstruction

Chronic infections

Causes suppurative destruction of renal tissue

Can lead to abscess formation

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118
Q

Bacteremia

A

Blood cultures are positive

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119
Q

Sepsis/septicemia

A

Suspected or documented infection and an acute increase in organ failure

Dysregulated host response to infection

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120
Q

Septic shock

A

Progressive organ dysfunction leading to marked increase in mortality

  • suspect of sepsis
  • serum lactate greater than 2mmol/L (18 mg/dL)
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121
Q

When does acute ischemia occur

A

Defect in effective circulating volume

  • decreased oxygen delivery
  • impaired removal of cellular waste
  • kidney receives 20-25% of CO

Couple whammy: direct tubular damage by endotoxins and inflammatory cytokines

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122
Q

Sepsis

A

Multiorgan involvement in infection removed from the source

Hypofunction of uninflected organs

Septic shock; hypotension that cannot be reversed with infusion of fluids

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123
Q

Shock: hypoperfusion regardless

A

Tachycardia
Hypotension
Tachypnea

Hypothermia/fever

Low oxygen-> celllular injury->inflammatory mediators-> worsening microvascular circulation

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124
Q

What history when shock

A

Trauma, recent surgery, signs of illness/infection

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125
Q

Three flow charts

A

Signs of inf

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126
Q

Septic shock signs

A

Infection sign: fever or hypothermia

Tachycardia: cardiac response to hypoperfusion and fever

Tachypnea: compensatory respiratory response

Hypotension!: sign of critical illness, responsive to fluid resuscitation
-how can you identify the source of infection

Circulating cytokines

Endothelial injury: decreased tone, increased permeability

Edema

Decreased oxygenation of tissues

Build up of lactic acid

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127
Q

Initiating treatment for sepsis/septic shock

A

Volume resuscitation (IV fluids)

Cultures: blood, urine, CSF,

Initiate antibiotics for most likely cause; generally broad spectrum

Pressers: norepinephrine, vasopressin, in addition for severe cases

Correct acid/base imbalance-fluids oxygenation(ventilator support)

Monitor electrolytes

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128
Q

Which is most important for treating sepsis/septic shock

A

Getting cultures or getting x ray lab results?

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129
Q

BUN :Cr sepsis and ischemia

A

Increase

-pre renal azotemia

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130
Q

FENa sepsis and ischemia

A

> 1%

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131
Q

Urine sepsis and ischemia

A

Decreased concentration

Proteinuria (minor)

Hematuria

Muddy brown casts on microscopy-sloughing of renal tubular epithelial. Cells

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132
Q

Prevent recurrent UTI: do it when they are interfering with patients lifestyle

A

Antibiotic therapy-continuous, post coital, patient initiated

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133
Q

Non medication preventative strategies for women

A

Empty bladder as soon as reasonable after intercourse

Wipe front to back

Shower not baths

Lactobacillus probiotics

Cranberry supplements

Vitamin c

Increase fluid intake!

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134
Q

Treat febrile UTI sepsis

A

Stabilize, resuscitate, treat with culture specific antibiotics for 2 weeks

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135
Q

Treat febrile UTI pyelonephritis

A

Treat with culture specific antibiotics 2 weeks

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136
Q

Treat non febrile UTI

A

Culture specific antibiotics 1 week

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137
Q

LO

A

Distinguish types of proteinuria and nephrotic syndrome

Develop a differential diagnosis for proteinuria based on pre disposing factors, clinical presentation, history and physical
Evaluate nephrotic range proteinuria

Recommend screening for proteinuria in patients with DM based on guidelines

Determine diagnostic approach for proteinuria

Discuss treatment strategies for diabetic nephropathy to prevent deterioration of renal function

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138
Q

Routine dipstick

A

Teststrip threshold is to turn positive for over 300 mg of albumen

Multiple types of proteins possible and multiple underlying causes

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139
Q

Quantify protein

A

Albumen Cr ratio

Can be done on random urine sample

Preferably first morning void

OR 24 hour urine collection-protein, albumen, Cr clearance
-also provides sample to do electrophoresis to determine which types of protein

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140
Q

Next step

A

Based on differential

DDx derived from thorough history and PE

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141
Q

Nephrotic range proteinuria vs nephrotic syndrome

A

Nephrotic syndrome-nephrotic range proteinuria, hyperlipidemia, hypoalbuminemia, edema

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142
Q

Screening recommendations

A

T2DM

-established diagnosisL annual ACR (albumen/Cr ratio)

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143
Q

Slow progression of proteinuria

A

Drug classes-ace inhibitors, arbs

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144
Q

Other possible causes of nephrotic syndrome

A

SLE, rheumatoid arthritis

Infection
0hepBC, HIV, syphilis, TB

Hematologists/oncologist
-amyloidosis, multiple myeloma, sickle cell, liquid and solid tumors

Drugs-NSAIDS, lithium, IV heroin

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145
Q

Routine dipstick

A

Teststrip threshold is to turn positive for over 300 mg of albumin

Multiple types of proteins possible and multiple underlying causes

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146
Q

Case 2

A

Ok

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147
Q

Exercise induced hematuria

A

50-80% of athletes

May also be accompanied by proteinuria

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148
Q

What does heavy exercise cause

A

Proteinuria

Decreased RBF leads to nephron ischemia, increased permeability , and subsequent passage of RBC

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149
Q

Who gets exercise issues

A

Swimmers, track, lacrosse

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150
Q

___ are common among athletes and another cause of microscopic hematuris

A

NSAIDS

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151
Q

Evaluate heavy exercise

A

Rule out infection

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152
Q

Treat heavy exercise

A

48-72 hours and recheck

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153
Q

NSAIDS how do they damage kidney

A

Inhibiting cyclooxygenase within the kidney

  • cyclooxygenase is the rate limiting enzyme for prostaglandins
  • PGE2 and PGI2 protect kidney by modulating renal vasoconstriction

Ibuprofen decreases GFR compared to placebo or acetaminophen

Indomethacin and celecoxib decreases free water clearance

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154
Q

Menstruation

A

Sloughingsee blood

History will help

Rule out infection

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155
Q

False positive dipstick

A

35%

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156
Q

UA false positives

A

Clean catch, mid strea,

-this eliminates urethral irritation and contamination from perineum

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157
Q

What else can give false positive

A

Myoglobinuria, hemoglobinuria
High alkaline (pH>9)
Ascorbic acid

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158
Q

How deal with false positives

A

Confirm with microscopy

Less than 3 RBBC/Hpv is negative for hematuria

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159
Q

Trauma of kidney common?

A

No due to location

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160
Q

What can traumatize the kidney

A

Blunt force, rapid deceleration

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161
Q

Who gets exercise issues

A

Swimmers, track, lacrosse

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162
Q

___ are common among athletes and another cause of microscopic hematuris

A

NSAIDS

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163
Q

Evaluate heavy exercise

A

Rule out infection

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164
Q

Treat heavy exercise

A

48-72 hours and recheck

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165
Q

NSAIDS how do they damage kidney

A

Inhibiting cyclooxygenase within the kidney

  • cyclooxygenase is the rate limiting enzyme for prostaglandins
  • PGE2 and PGI2 protect kidney by modulating renal vasoconstriction

Ibuprofen decreases GFR compared to placebo or acetaminophen

Indomethacin and celecoxib decreases free water clearance

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166
Q

Menstruation

A

Sloughingsee blood

History will help

Rule out infection

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167
Q

False positive dipstick

A

35%

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168
Q

UA false positives

A

Clean catch, mid strea,

-this eliminates urethral irritation and contamination from perineum

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169
Q

What else can give false positive

A

Myoglobinuria, hemoglobinuria
High alkaline (pH>9)
Ascorbic acid

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170
Q

How deal with false positives

A

Confirm with microscopy

Less than 3 RBBC/Hpv is negative for hematuria

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171
Q

Trauma of kidney common?

A

No due to location

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172
Q

What can traumatize the kidney

A

Blunt force, rapid deceleration

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173
Q

How does renal trauma present

A

Hematuria
(But lack doesn’t exclude)

Evidence of rib fracture

Guided on suspicion

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174
Q

Radiographically evaluation kidney trauma

A

Not if hemodynamically stable

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175
Q

Sickle cell screening

A

At birth
History is often lost, forgotten

Single hemoglobin S mutation

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176
Q

What does sickle cell cause

A

Impaired urinary concentration

Can develop renal papillary necrosis

Hyperfiltration elads to albuminuria, interstitial fibrosis, decreased number of nephrons

RENAL MEDULLARY CARCINOMA

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177
Q

Males at risk for transitional cell and bladder cancer

A 
Males
>35
Current or past smoker
Analgesic
Exposure to chemicals or dyes
Exposure to carcinogenic agents or chemo
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178
Q

Other history of cancer

A 
Gross hematuria
Urologic disorder or disease
Irritation voiding symptoms
-what does this mean?
Pelvic irradiation
Chronic urinary tract infection chronic indwelling
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179
Q

Diagnosis of BHP should not preclude further evaluation of underlying cause

A

Huh

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180
Q

How evaluate malignancy

A

Know risk

Rule out infection with culture and sensitivity

Confirm with microscopy

Serum BUN Cr

Radiographically

US VC CTU

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181
Q

US

A

No radiation
Low cost
May miss other causes of hematuria: small stones, small bladder mass and urothelial transitional cell carcinoma

Very good for tumors >3cm, cysts, and hydronephrosis

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182
Q

CTU

A

CT or kidney, ureters, and bladder

With or without contrast

Sensitive for renal calculi!

Able to detect small renal parenchymal masses, aneurysm, and renal and perirenal abscesses

Higher radiation

Exposure to contrast agents

Higher cost

More info

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183
Q

Cytoscope

A

Evaluate bladder by direct visualization

Better assessment of bladder wall for microstructiral changes

Can identify urethral stricture disease, BHP and bladder masses

Invasive, requires sedation, risk for UTI

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184
Q

Recommendations for cytoscopy

A

Vary
Primary care: after negative US or IVP

AUA: all patients >35 with asymptomatic microhematuria

Or all patients with risk factors for urologic malignancies regardless of age

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185
Q

Chronic glomerulonephritis

A

Glomerular scarring

Corticular tubular atrophy

Interstitial inflammation

Interstitial fibrosis

Atherosclerosis

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186
Q

Vascular/ hemodynamics effect of RAAS

A

Vasoconstriction of affferent and efferent and systemic arterioles

Increases glomerular pressures

Causes direct glomerular damage

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187
Q

Inflammatory effects of RAAS

A

Activated inflammatory system

Leads to interstitial and tubular fibrosisi

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188
Q

Glomerulonephritis

A

Hematuria
-microscopic vs gross

Proteinuria
-albumineria vs protein

Acute vs chronic

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189
Q

How tell acute vs chronic glomerulonephritis

A

HISTORY
Genetic disorders, systemic disease
Family history of lupus, sickles cell, autoimmune, diabetes, coronary artery

Recent infectionsL staph, malaria, schistomiasis

Infection HIC hep BC

ROS-itching, nausea, headache, anorexia, dyspnea, vomiting, diarrhea, hiccup, restlessness and depression

UA and chemistry

US-for size

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190
Q

Size of kidney in chronic disease

A

Smaller

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191
Q

Hematuria glomerulonephritis

A

Asymptomatic can be 3-5 RBC

RBC casts or dystrophic

Gross hematuria in sickle or IgA nephropathy

Always get UA with microscopy to verify findings

Culture and sensitivity to rule out infection

Microscopic hematuria needs to be differentiated from anatomic lesions-BPH, tumors, stones

Pyruvate in inflammatory glomerulonephritis and should be differentiations from UTI

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192
Q

Acanthocytes

A

Contracted, dense irregular

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193
Q

Dystrophic

A

Mickey Mouse

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194
Q

RBC have lost typical disc shape indicating what

A

Moved through nephron not just the Collecting system

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195
Q

Proteinuria sustained

A

1-2 g/24 h

Symptoms of edema and foamy urine

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196
Q

Benign proteinuria

A

Functional or transient
<1-2 g/24 hours

Fever, exercise, obesity, sleep apnea, emotional stress and CHF

Orthostatic proteinuria-only occurs with standing

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197
Q

24 hours albumin in normal, microalbuminuria and proteinuria

A

8-10

30-300

> 300

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198
Q

Albumin/creatinine ratio

Normal, microalbuminuria, proteinuria

A

<30
30-300
>300

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199
Q

Dipstick microalbuminuria proteinuria

A

+1

+3

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200
Q

24 hour protein normal proteinuria

A

<150

>150

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201
Q

Send for UA with microscopic evaluation

A

+15 dystrophic RBC

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202
Q

Return to office

A

Review BP log
Initiate antihypertensice-low fat sodium diet

Diabetic protocol

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203
Q

What is the mechanism of damage in hypertensive nephropathy

A

Ok

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204
Q

Hypertensive nephrosclerosis

A

Five times more common in black

APOL1 increased risk in black

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205
Q

Other risk of hypertensive nephrosclerosis

A

Smoking, male, hyerclorestelemia, HTN, low birth weight and preexisting renal injury

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206
Q

Signs hypertensive nephrosclerosis

A

HTN, microhematuria and moderate proteinura

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207
Q

Why blood pressure control with hypertensive nephrosclerosis

A

Delays progression to end stage renal

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208
Q

Diabetic nephropathy

A

Damage related to extracellular matrix accumulating in both GBM and tubular BM

Imbalance between synthesis and degradation of the ECM causes expansion of mesangial

The glomerular filtration surface is decreased by the reduced glomerular luminal space with leads to the reduction in GFR

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209
Q

Type 1 glomerular, tubular, interstitial and vascular lesions tend to progress more or less in parallel and independent of albuminuria

A

Type 2 variable in progression and can develop albuminuria with little change to the nephron

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210
Q

Both present how

A

Clinically stable. Edema and worsening HTN are late findings

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211
Q

What can traumatize the kidney

A

Blunt force, rapid deceleration

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212
Q

How does renal trauma present

A

Hematuria
(But lack doesn’t exclude)

Evidence of rib fracture

Guided on suspicion

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213
Q

Radiographically evaluation kidney trauma

A

Not if hemodynamically stable

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214
Q

Sickle cell screening

A

At birth
History is often lost, forgotten

Single hemoglobin S mutation

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215
Q

What does sickle cell cause

A

Impaired urinary concentration

Can develop renal papillary necrosis

Hyperfiltration elads to albuminuria, interstitial fibrosis, decreased number of nephrons

RENAL MEDULLARY CARCINOMA

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216
Q

Males at risk for transitional cell and bladder cancer

A 
Males
>35
Current or past smoker
Analgesic
Exposure to chemicals or dyes
Exposure to carcinogenic agents or chemo
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217
Q

Other history of cancer

A 
Gross hematuria
Urologic disorder or disease
Irritation voiding symptoms
-what does this mean?
Pelvic irradiation
Chronic urinary tract infection chronic indwelling
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218
Q

Diagnosis of BHP should not preclude further evaluation of underlying cause

A

Huh

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219
Q

How evaluate malignancy

A

Know risk

Rule out infection with culture and sensitivity

Confirm with microscopy

Serum BUN Cr

Radiographically

US VC CTU

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220
Q

US

A

No radiation
Low cost
May miss other causes of hematuria: small stones, small bladder mass and urothelial transitional cell carcinoma

Very good for tumors >3cm, cysts, and hydronephrosis

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221
Q

CTU

A

CT or kidney, ureters, and bladder

With or without contrast

Sensitive for renal calculi!

Able to detect small renal parenchymal masses, aneurysm, and renal and perirenal abscesses

Higher radiation

Exposure to contrast agents

Higher cost

More info

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222
Q

Cytoscope

A

Evaluate bladder by direct visualization

Better assessment of bladder wall for microstructiral changes

Can identify urethral stricture disease, BHP and bladder masses

Invasive, requires sedation, risk for UTI

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223
Q

Recommendations for cytoscopy

A

Vary
Primary care: after negative US or IVP

AUA: all patients >35 with asymptomatic microhematuria

Or all patients with risk factors for urologic malignancies regardless of age

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224
Q

Chronic glomerulonephritis

A

Glomerular scarring

Corticular tubular atrophy

Interstitial inflammation

Interstitial fibrosis

Atherosclerosis

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225
Q

Both present how

A

Clinically stable. Edema and worsening HTN are late findings

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226
Q

Type 1 glomerular, tubular, interstitial and vascular lesions tend to progress more or less in parallel and independent of albuminuria

A

Type 2 variable in progression and can develop albuminuria with little change to the nephron

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227
Q

Diabetic nephropathy

A

Damage related to extracellular matrix accumulating in both GBM and tubular BM

Imbalance between synthesis and degradation of the ECM causes expansion of mesangial

The glomerular filtration surface is decreased by the reduced glomerular luminal space with leads to the reduction in GFR

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228
Q

Why blood pressure control with hypertensive nephrosclerosis

A

Delays progression to end stage renal

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229
Q

Signs hypertensive nephrosclerosis

A

HTN, microhematuria and moderate proteinura

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230
Q

Other risk of hypertensive nephrosclerosis

A

Smoking, male, hyerclorestelemia, HTN, low birth weight and preexisting renal injury

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231
Q

Hypertensive nephrosclerosis

A

Five times more common in black

APOL1 increased risk in black

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232
Q

What is the mechanism of damage in hypertensive nephropathy

A

Ok

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233
Q

Return to office

A

Review BP log
Initiate antihypertensice-low fat sodium diet

Diabetic protocol

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234
Q

Send for UA with microscopic evaluation

A

+15 dystrophic RBC

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235
Q

24 hour protein normal proteinuria

A

<150

>150

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236
Q

Dipstick microalbuminuria proteinuria

A

+1

+3

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237
Q

Albumin/creatinine ratio

Normal, microalbuminuria, proteinuria

A

<30
30-300
>300

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238
Q

24 hours albumin in normal, microalbuminuria and proteinuria

A

8-10

30-300

> 300

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239
Q

Benign proteinuria

A

Functional or transient
<1-2 g/24 hours

Fever, exercise, obesity, sleep apnea, emotional stress and CHF

Orthostatic proteinuria-only occurs with standing

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240
Q

Proteinuria sustained

A

1-2 g/24 h

Symptoms of edema and foamy urine

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241
Q

RBC have lost typical disc shape indicating what

A

Moved through nephron not just the Collecting system

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242
Q

Dystrophic

A

Mickey Mouse

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243
Q

Acanthocytes

A

Contracted, dense irregular

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244
Q

Hematuria glomerulonephritis

A

Asymptomatic can be 3-5 RBC

RBC casts or dystrophic

Gross hematuria in sickle or IgA nephropathy

Always get UA with microscopy to verify findings

Culture and sensitivity to rule out infection

Microscopic hematuria needs to be differentiated from anatomic lesions-BPH, tumors, stones

Pyruvate in inflammatory glomerulonephritis and should be differentiations from UTI

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245
Q

Size of kidney in chronic disease

A

Smaller

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246
Q

How tell acute vs chronic glomerulonephritis

A

HISTORY
Genetic disorders, systemic disease
Family history of lupus, sickles cell, autoimmune, diabetes, coronary artery

Recent infectionsL staph, malaria, schistomiasis

Infection HIC hep BC

ROS-itching, nausea, headache, anorexia, dyspnea, vomiting, diarrhea, hiccup, restlessness and depression

UA and chemistry

US-for size

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247
Q

Glomerulonephritis

A

Hematuria
-microscopic vs gross

Proteinuria
-albumineria vs protein

Acute vs chronic

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248
Q

Inflammatory effects of RAAS

A

Activated inflammatory system

Leads to interstitial and tubular fibrosisi

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249
Q

Vascular/ hemodynamics effect of RAAS

A

Vasoconstriction of affferent and efferent and systemic arterioles

Increases glomerular pressures

Causes direct glomerular damage

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250
Q

Issue with kidney

A

Effects every part in the body

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251
Q

Hyperfiltration

A

Kidneys beat themselves up when not functioning

Usually starts with AKI-damage to nephrons-problem linked to how quickly you turn around and co morbididies

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252
Q

What happens with hyperfiltration

A

Sclerosis, damage to nephron, lose function,

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253
Q

RAAS

A

Originally protective

Then damaging

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254
Q

How RAAS hurt

A

Build up in kidney with chronic kidney disease

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255
Q

Most common disease to cause kidney damage

A

Diabetes then HTN

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256
Q

Acute injury renal injury/failure related to what

A

Rise in Cr

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257
Q

Normal GFR

A

90, 100

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258
Q

Stage 2 AKI

A

GFR 60-89

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259
Q

Stage 3

A

30-59

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260
Q

Stage 5

A

Less than 15 for GFR

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261
Q

Stage 2

A

HTN that starts to get harder to control,

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262
Q

Stage 3

A 
Increase Parathyroid hormone (doesn’t get filtered out)
Bone effects (calcium, P, Mg)
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263
Q

Stage 4

A

Acidosis

Changes in K

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264
Q

Stage 5

A

Uremic syndrome

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265
Q

Na

A

Decrease Na excretion in dysfunctional kidney, making more water hang around, goes into third spaces (non vascular non cellular)->dependent edema easrly(becomes systemic later on)

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266
Q

Why will Na labs be in normal range

A

Bc extra water

Use diuretics

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267
Q

K

A

Doesn’t change a lot till late stages unless high intake or start pharmacologically getting rid of it (loop diuretics)
RAAS system

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268
Q

How one increase K

A

Foods-sweet potato

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269
Q

Acidosis

A

Once start losing functional nephrons (LOSS OF NEPHRONS IS PROBLEM) bc related to ammonia production

Initially hyperchloremia acidosis NAGMA at gfr 40

Then HAGMA bc of retained organic anions—— GFR 15 20 HAGMA

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270
Q

Late stages kidney disease

A

Catabolic state
Get sicker and sicker
*acidosis of kidney-inadequate ammonium production

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271
Q

Signs of uremia

A

Fatigue, anorexia, vomiting, hiccup, metallic taste

Hwy?changes in hormone an electrolytes
Chronic inflammation-

Really sick-effect bone, blood skin -effects everything

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272
Q

Late stage 3 changes uremia

A

Decreased P excretion, PTH and growth of parathyroid, D3 down, all effecting bone!

Hyper parathyroid-muscle weakness and fatigue, malaise, low energy

High turn over-fibrosis cystica-bone cysts, soft bones more likely to break (not recycling)

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273
Q

Without bone turnover

A

Lots of mineralization defects

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274
Q

Symptoms chronic kidney

A

HyperP?
HypoCa
HypoVD

Secondary hyperparathyroidism

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275
Q

Loss of nephron mass

A

Triggers cascade
Some decreased renal biosynthesis-vitamin D

Decreased VD-hypoCa (gut function)

Hyper P changes in excretion

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276
Q

Hyper P

A

Capture Ca so get P Ca complex and deposit in soft tissue

PTH keeps goes up

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277
Q

Parathyroid

A

Cardiac muscle fibrosis

Changes in flow bc CO

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278
Q

P up Ca down treat

A

Exogenous VD

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279
Q

Do people die of renal failure

A

No atherosclerosis changes in heart kill them

All related to inflammatory state

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280
Q

Patient with chronic renal disease

A

Cholesterol levels, have a better lifestyle , lose weight

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281
Q

Symptoms uremia

A

Fatigue, decreased appetite, malaise

CAREFULLY MANAGE

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282
Q

Anemia AKI

A

Associated with changes in EPO or bone marrow fibrosis

Dysfunctional platelets and decreased immune function

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283
Q

Normochronmic normocitic anemia how long do the red cells live

A

Not as long

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284
Q

Neocytolysis

A

Changing and destroying red cells

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285
Q

Anemia leads to what symptoms

A

Fatigue, decreased exercise tolerance, decrease cognition, heart hypertrophy(but parathyroid making it fibrose)

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286
Q

Can we replace EPO

A

Yup increase red cell count

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287
Q

Neuromuscular changes AKI when

A

Drop to 30-44

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288
Q

Effects neuromuscular

A

Cramping hicccups

Neuropathy lower extremities first more sensory then becomes motor

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289
Q

GI effects AKI

A

Uremic fetter-urine breath

Gastricis
PUD
Don’t want to eat
Vomit
Constipation

Catabolic state-

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290
Q

Treat AKI

A

Protein restriction Na restict——-but become calorie depleted

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291
Q

Insulin AKI

A

Increased plasma cells-largely excreted by kidney so if around longer prob

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292
Q

AKI testosterone and estrogen

A

Young woman-decreased estrogen and problems bearing children, irregular menstrual cycles, on top of bone disease

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293
Q

Kid CKI

A

Growth retardation failure to thrive

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294
Q

Skin changes

A

Hyperpigmentation
Pigments not filtering out

Will look spray on tanned-skin gets itchy as P up

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295
Q

Why chronic itching

A

P up

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296
Q

Treat AKI

A

Monitor BP
ACE and ARB(we have dysfunctional RAAS)

Monitor volume, volume can be measured in a lot of ways
-daily weight check

Na restrict-canned food

Avoid nephrotoxicity drug-anti inflammatory-IBUEPROFIN AND ALEVE EFFECT KIDNEY BC DONT FEEL WELL AND MORE TAKE MORE DAMAGE DO

Gentamycin

Contrast agents-CT skan? Catch lab? Iodine based bad

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297
Q

When a person gets to stage 4

A

Send to nephrologist GFR less than 30
Nephrolegist on board

Build relationship between attention and nephrologist bc if continue to more forward and need transplant and dialysis-

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298
Q

Dialysis types

A

Emergent-if no urine, can be short term-port in neck, can be used temporality maybe week or 2 at most

Peritoneal-uses abdominal cavity and lining as membrane-insert hyperosmolar solution with large amount of glucose or sugar creating osmotic gradient to pull solvents across and some albumin comes -leave till become steady state then flush it out

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299
Q

Complications peritoneal dialysis

A

Hernia
Avenue for infection

Can do at bedtime at night get flow then excreted in morning

Can do hourly

Not as reliable and failure rates are high-omentum can sclerosing and cause obstruction of GI
Solution is sugar so diabetic need to adjust insulin

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300
Q

Sclerosing encapsulating peritonitis

A

Peritoneal dialysis

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301
Q

External hemodialysis

A

Fistula in forearm join an artery and vein they will vibrate bc of change in pressure-palpable thrill

Blood out run though so solute move across membrane taking 4-6 hours then back in

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302
Q

Transplant list

A

Can’t have active malignancy, infection, CV and pulmonary evaluation

If any other underlying disease move further and further down on list

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303
Q

As kidney fail the ___

A

Shrink

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304
Q

How do transplant

A

Put kidney low in abdomen connect o iliac artery and create a ureter.

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305
Q

GFR 30

A

Send to nephrology

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306
Q

GFR15 or less

A

Dialysis transplant

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307
Q

Pediatric renal topics

A

Ok

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308
Q

Kids with HTN

A

End organ damage

Kidney

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309
Q

Normal BP in kid

A

Less than 90th percentile

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310
Q

When start check bp in kid

A

3

Unless risk factor-premature, known renal disease

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311
Q

How many times have to do bp to say someone is htn

A

Blood pressure over 90th percentile at three different visits

312
Q

Primary vs secondary

A

Systolic high

Systolic and diastolic high

313
Q

White coat

A

Up, from stress of doctor

Measure bp outside of clinical settting is important

314
Q

Ambulatory measure

A

Good

315
Q

Diastolic

A

Sound disappear

316
Q

If found never goes away use 4th

A

Ok

317
Q

ECG good enough to say if there is left ventricular hypertrophy

A

Establishment of cronicity of high bp!!!!!!

318
Q

Too small

A

High bp

319
Q

Too big

A

Low bp

320
Q

Hematuria

A

3-5 RBC per high power field (microscopic)

321
Q

How many blood cells to turn urine red

A

A ton hundreds of thousands

322
Q

Urine dipstick positive for blood

A

Myoglobin, hemoglobin (need to determine which? Rhabdo-myoglobin is devastating to the kidneys-happens a lot in army bases get rhabdoid and get liters of IV fluid to keep kidney working)

323
Q

Does positive dipstick tell you if RBC in urine in tact

A

No
Need to do microscopy
-

324
Q

Color urine babies

A

Uric acid crystals-red brick colorjust hydration will make it go away

Bilirubin

325
Q

If want to confirm blood of urine is from blood

A

Look under microscope

326
Q

Glomerular bleeding

A

RBC dysmorphic

327
Q

Bleeding along urinary tract

A

More normal appearing

328
Q

Blood in urine

A

Is there protein? Protein with blood is diagnostic for…

329
Q

Post strep glomerulonephritis kids

A

Edema, urine dark, gross hematuria, elevated ASO, serum compliment low (used up in immune complex forming)

330
Q

Lupus

A

Glomerulonephritis

331
Q

Most common cause of glomerulonephritis in lupus

A

MPGN

332
Q

Henoch schonlein purpura

A

Bruise then come in with lots of them

  • usually after viral(cold)
  • immune complex vasculitis, IgA
  • gross hematuria
  • ab pain
  • intestinal vasculature
  • really sick
333
Q

Every kid with henoch

A

Blood in urine

If blood and protein-SIGNIFICANT-progress to end stage renal failure

We know blood there, but if protein then nephrologist involved

334
Q

Rarely kids with asymptomatic isolated hematuria

A

Have prob

Usually goes away

But monitor for protein and and htn

335
Q

UTI kids

A

Same signs and symptoms BUT cant tell you anything, if not potty trained harder

336
Q

Fever and cant find source of infection

A

Always urine in kids espicially if non verbal

337
Q

Best way to get urine sample from kids

A

Catheter or suprapubic tap-used in neonates(rarely newborns or young infants)

Bag urine-negative fine , but if positive cant send bag in for culture bc contaminants, so gotta do catheter or suprapubic tap

338
Q

Urine nitrate testing on dipstick

A

Some bacteria change nitrates to nitrites

So positive nitrites indicative of bacteria present

339
Q

Most common bacterial pathogen for kid UTI

A

E. coli

340
Q

Treat

A

Cephalosporin is standard

If too sick use parenteral or IV or shot

341
Q

When image kid urinary tract

A

After first UTI in boys
Get renal and bladder US
And VCUG

Girls-first UTI both renal US and renal UCVG if symptoms of chronic renal disease or HTN ….
weird pathogen

Second or third if no other symptoms of renal disease

342
Q

AKI

A

Onset days increase in serum Cr

Volume of output decreases

343
Q

What can alter serum Cr

A

Age
-less muscle mass

, sex, race, muscle mass, catabolic rate

344
Q

AKI prognosis

A

50% mortality

345
Q

Acute non chronic

A

Obtain the most recent serum cr

346
Q

Pre renal

A

Affects kidney
How it originates

Dehydration, fluid shift into different place in body from heart or liver problems, NSAIDS,

347
Q

Intrinsic

A

Renala glomerular, tubulointerstitial/interstitial

Vascular-vascultis/rheumatologist, malignant HTN, TTP HUS

348
Q

Tubulointerstitial causes

A 
Ischemia
Sepsis/infection
Exogenous nephrotoxicity
-iodinated contrast
-aminoglycosides, amphotericin B, cisplastin, PPI, NSAIDS
349
Q

OTC PPI, NSAIDS

A

Make sure know herbal, vitamin

350
Q

Endogenous nephrotoxicity

A

Hemolysis, rhabdomyolysis (myoglobin), myeloma, intratubular crystals

351
Q

Flu, running

A

Rhabdomyolysis

352
Q

Dipstick rhabdomyolysis

A

Positive blood, but its not blood-its myoglobin! Make sure get microscopic.

353
Q

Myeloma

A

Tylenol 3 lots post phoned diagnose cancer

-

354
Q

Post renal AKI

A

Bladder outlet obstruction

Bilateral pelvoureteral obstruction

355
Q

History

A

all medications

Toxins-work/home
-lead,

PMH/PSH?ROS

356
Q

Physical signs AKI

A

Dehydration, ascites, jaundice, fluid in lungs

357
Q

What order

A

Serum na and cr

Urine na and cr

358
Q

Why order serum and urine na and cr

A

FENa.

359
Q

When order UA with micro

A

Don’t get Cr and Na

360
Q

Need BMP and urine specified Na and Cr

A

For pre post or intrinsic important o order

361
Q

For AKI why use K and Cl

A

Anion gap

362
Q

Hemoglobin and hematocrit CBC, platelet count

A

Need may be changes

363
Q

Coagulation time

A

PT TPP
May lead to liver problem if have ascites

If have to do procedures or biopsy if put in dialysis catheter need to know

364
Q

Ekg

A

See if k problem going on

365
Q

Treat presok

A

Ok

366
Q

Night before fulllness suprapubically size of golf ball no fever

A

Flocked fluids

367
Q

Routing dipstick

A

Positive if 300 mg of albumin

Multiple types of protein though and multiple underlying causes

368
Q

Negative dipstick

A

Doesn’t mean have no albumin

369
Q

UA

A

Get dipstick

370
Q

UA and micro

A

Dipstick and microscopic evaluation-casts, cells, bacteria

371
Q

Next step

A

Quantify

ACR-albumin/Cr ration

372
Q

Spot urine

A

Random urine sample

373
Q

Best urine

A

First morning , bc false negative increases as patient takes in more fluid

374
Q

24 hour urine

A

Protein, albumin, Cr clearance

Sample that need for electrophoresis-tell what type of protein , has to be on 24 hours urine

375
Q

Issue with 24 hour urine

A

Lot of urine
Containers to store
Arthritis in hands
Store on ice

376
Q

Other possible next steps

A

Based on differential

DDX derived from thorough history and PE

377
Q

Blood test

A

Albumin eleven

378
Q

Chemistry panel

A

Electrolytes, lipid(must specify), blood sugar

379
Q

Blood count CBC

A

Hemoglobin hematocrit

If have protein in urine -kidney primary MCD or a secondary cause (anemic and chronic disease)

Platelets

380
Q

What systemic disease effect the kidney

A 
Lupus
Rheumatologist disorders
-ANA for possible lupus 
-CHF look at CMP 
-chest x ray see if fluid in pulmonary

Not having these symptoms yet still check

381
Q

Syndrome

A

Constellation of problems

382
Q

Nephrotic range proteinuria

A

Large amount of protein 3.5 g/3500 mg

383
Q

Negative dipstick

A

Doesn’t mean have no albumin

384
Q

UA

A

Get dipstick

385
Q

UA and micro

A

Dipstick and microscopic evaluation-casts, cells, bacteria

386
Q

Next step

A

Quantify

ACR-albumin/Cr ration

387
Q

Spot urine

A

Random urine sample

388
Q

Best urine

A

First morning , bc false negative increases as patient takes in more fluid

389
Q

24 hour urine

A

Protein, albumin, Cr clearance

Sample that need for electrophoresis-tell what type of protein , has to be on 24 hours urine

390
Q

Issue with 24 hour urine

A

Lot of urine
Containers to store
Arthritis in hands
Store on ice

391
Q

Other possible next steps

A

Based on differential

DDX derived from thorough history and PE

392
Q

Blood test

A

Albumin eleven

393
Q

Chemistry panel

A

Electrolytes, lipid(must specify), blood sugar

394
Q

Blood count CBC

A

Hemoglobin hematocrit

If have protein in urine -kidney primary MCD or a secondary cause (anemic and chronic disease)

Platelets

395
Q

What systemic disease effect the kidney

A 
Lupus
Rheumatologist disorders
-ANA for possible lupus 
-CHF look at CMP 
-chest x ray see if fluid in pulmonary

Not having these symptoms yet still check

396
Q

Syndrome

A

Constellation of problems

397
Q

Nephrotic range proteinuria

A

Large amount of protein 3.5 g

398
Q

Nephrotic syndrome

A

Need proteinuria
Hyperlipidemia-fasting cholesterol/lipids
Hypoalbuminemia
Edema

399
Q

63 yo male polyuria polydipsia (drinking a lot) and facial swelling for 3 months.

A

Anytime patient thirsty or urinating a lot

-tip off for diabetes (losing sugar and fluid-osmotic diuretic)

400
Q

What is DM associated with

A

Nephrotic syndrome-may cause it

Hypoalbuminemia

401
Q

Why low albumin in blood stream and spilling protein in urine cause swelling

A

Lose colloid osmotic so leak out interstitial then think low so raas

402
Q

DM with edem

A

Most likely effecting kidney

403
Q

Drug decrease proteinuria

A

ACE ARB

404
Q

Type II DM

A

Annual ACR (albumen/Cr ratio)

405
Q

lupus and rheumatoid arthritis and nephrotic syndrome

A

Ok

406
Q

Infection nephrotic

A

Hep BC-cryoglobinuremia

HIV
Syphilis

Tuberculosis

407
Q

HIV

A

Focal segmental glomerulosclerisus

408
Q

Hematologic/oncologist cause of nephrotic

A

Amyloidosis
Multiple myeloma
Sickle cell
Liquid and solid tumors

409
Q

Drugs cause nephrotic

A

NSAIDS
Lithium
IV heroin

410
Q

72 year old male severe back pain for year. Works a small farm. No specific identifiable injury. He works in hostpital. Couple different physician give pain pill on separate occasion, not aware of other. Tylenol 3.

A

Hazards of opoids. Codeine is controlled. Any prescription should be done with caution.
They didn’t do PE, no chart, they just gave him pills.
Huge risk to patient and postponed care

411
Q

What else might patient take with this constellation

A

NSAIDS twice the recommended

412
Q

Effect

A

Proteinuria
-as did evaluation, did 24 hour urine to quantify and get protein electrophoresis bc his age group prone to multiple myeloma-he has indirectly transposed treatment to malignancy

413
Q

AAFP article on hematuria in adult

A

Ok

414
Q

22 yo male going to do triathlon needs physical before . Runs and does weight. He has 1+ blood

A

Hematuria in athletics

Heavy exercise induce hematuria in 80% of athletes and may have proteinuria

415
Q

Why

A

Exercising heavily, get renal ischemia for short periods of time. Result in red cells in urine. More common in swimmers, track, and lacrosse.

416
Q

Athletes have pains

A

Take NSAIDS

Also can cause hematuria

417
Q

Take home message

A

Occult hematuria always get a microscopy and a culture and sensitivity
Then re check

418
Q

Why need microscopy

A

See where cellls come from

419
Q

NSAIDS

A

Inhibit COX in kidney ibueprofin bigger offender than acetaminophen

In drug classes have variation

Net effect of renal ischemia activates RAAS*** vasoconstriction

420
Q

RAAS from NSAID

A

Up up vasoconstrict

421
Q

26 yo female ab paina fter meal better if eat tums

UA-2+ blood

A

Menstruation give false positive up to 24 hours realize starting mesntral cycle and can persist for several days after

Need UA epigastric pain? No

422
Q

Dipstick false positive

A

Up to 35% false positive

423
Q

UA how collect

A

Mid stream mid catch, wash urethra this eliminates debris around urethra that would give false information

424
Q

Myoglobin in urin

A

Give heme positive result false positive in dipstick

425
Q

Ph>9 urine, certain types of proteus infection get

A

False positive

426
Q

Vitamin C false positive

A

Can give false positive in cold a flu season can get this

427
Q

What is hematuria

A

3 RBC per high powered field

428
Q

19 yo male presents with blood in urine. Plays football was struck from right and has bruise since then urine darker than usual but has continued to play foot ball 1+ blood 2+ urobilinogen

A

Kidney protected can just observe these patients and re check in 48 to 72 hours.

Need US depending on history and physical
Falls and rapid deceleration injuries hurt kidney?

429
Q

If they are hemodynamics stable do not need a US or CT to look at kidney

A

Ok

430
Q

22 yo african American male need veal so can play college basketball . Exam normal. 6’7
2+ blood

A

Sickle cell trait

431
Q

Sickle cell trait

A

Infants screened at birth
If not causing problem then, don’t worry

Can get renal papillary necrosis and get focal segmental glomerulonephropsis-RENAL MEDULLARY CARCINOMA

432
Q

What cancer worry about with sickle cell trait

A

Renal medullary carcinoma

433
Q

What do

A

Send for UA and culture and sensitivity

434
Q

55 yo male comes for refill bp meds. Former smoker quick when given high BP 1+ blood . UA neg for blood and protein a year ago

A

Probably cancer related to smoking

435
Q

Number one risk for bladder cancer

A

Smoking

436
Q

Other question

A

How much NSAIDS

Other exposures

437
Q

Gross hematuria painless

A

CANCER until proven otherwise

438
Q

Irritation voiding symptoms with hematuria

A

Dysuria, urgency, frequency

Tips balance away from cancer-

439
Q

What could have

A

Catheter, chronic UTI, pelvic irritation, schistosomiasis

440
Q

Blood with urine

A

Also microscopy and culture and sensitivity and

Get BUN, Cr serum eval

Radiographically?

441
Q

US

A

No radiation cheaper

Less sensitive for smalls tones, small bladder mass, good for hydronephrosis!!!

442
Q

CTU

A

2 phase radiographically test sensitive for renal calculi bc done in two phases

Expensive , radiation,

443
Q

CTU. Work

A

1st scan wo contrast second with

444
Q

Cytoscopy

A

Direct visualization if sure its a lower GU how we go in to get renal stones

If stone can get with basket , can get biopsy, can cauterize active bleeding, it is invasive (risk UTI and different thought)

445
Q

US or IVP negative

A

Can go straight to cystoscopy

446
Q

RBC gone through glomerulus

A

Dysmorphic

447
Q

Rbc from down

A

Looks fine

448
Q

Chronic glomerulonephritis

A

Scarring

Cortical tubular atrophy

Interstitial inflammation

Interstitial fibrosis

Atherosclerosis

449
Q

RAAS effect

A

Vasoconstriction

Increase

450
Q

50 yo male quick smoking last week when brother died from heart attack. Works for postal service, no exercise. What are his risk factors

A

Male
Smoker (non smoker until haven’t touched for 6 months)
Diet
Obese
No exercise
2+ edema
Prolonged expiration-typical of obstructive disease
Bilateral carotid bruits
Sinus rhythm with left ventricular hypertrophy and no t wave abnormalities

451
Q

What’s wrong with this guy

A

Atherosclerosis , HTN,

452
Q

What get

A

24 hour urine and BUN, Cr, Na, 24 hour urine

453
Q

Glomerulonephritis

A

Hematuria)microscopic vs gross)

Have some degre of proteinuria

454
Q

Acute vs chronic glomerulonephritis

A

Detailed history

Renal US-chronic kidney smaller

455
Q

All nephropathy

A

Give some hematuria

456
Q

Red cell casts or sysmorphic

A

Glomerulonephritis

As few as 3-5

457
Q

Sustained proteinuria

A

> 1-2 g/24 hours

Edema and or foamy urine

458
Q

Benign proteinuria

A

Functional or transient
1-2 g/24

Fever exercise, orthostatic

459
Q

Treat

A

Low fat diet and salt reduction

Exercise lose weight

460
Q

MOA in HTN nephropathy

A

RAAS and hyperfiltration

HTN initiate RAAS and glomerulus comes under pressure with hyperfiltration from changes and fibrosis

461
Q

Hypertensive nephrosclerosis who gets

A

African americans-young

All old people

462
Q

POL1

A

In black people

463
Q

Risk factors for hypertensive nephrosclerosis

A

Smoking, HTN< low birth weight, preexisting renal injury

464
Q

Signs hypertensive nephrosclerosis

A

HTN, microhematuria and moderate proteinuria

465
Q

How control progression

A

BP

466
Q

Diabetic nephropathy

A

ECM damage changes the glomerular filtration surface makes more leaks.

467
Q

Type I vs Type 2 diabetics

A

1-changes in parallel independent of albuminuria
2-develop albuminuria without changes to nephron

Both present with edema and worsening of HTN are late findings and related to LOSS OF NEPHRONS NOT CHANGE IN GLOMERULUS

468
Q

Changes in flow

A

Ok

469
Q

Initial phase obstruction of unilateral obstruction

A

Urine backflow-increases intraluminal hydrostatic pressure

A simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR

Activation of RAAS leads to the second phase

470
Q

Second phase 6 hours

A

Decrease glomerular blood flow due to afferent arterioles vasoconstriction

471
Q

Third phase unilateral

A

Decreased luminal hydrostatic pressure and renal blood glow below baseline

472
Q

Persistence unilateral obstruction>24 hours can cause what

A

50% drop in GFR

473
Q

US

A

Solid white fluid black

474
Q

Inject dys to find obstruction

A

Dye see how dilated ureter is in unilateral obstruction

475
Q

Bilateral 2 phases

A

Initial-urine backflow-increases intraluminal hydrostatic pressure
-simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR

RAAS is activated which leads to second phase

476
Q

Second phase bilateral

A

Decrease glomerular blood flow due to afferent arterioles vasoconstriction maintains GFR

477
Q

Why just two phases

A

ANP may maintain GFR and arteriolar function

478
Q

Tubular dysfunction unilateral

A

Inability to reabsorbed sodium
Salt eating

Downregulation of receptor and anxyme activity

Have high salt regular urine from the one kidney

479
Q

Tubular dysfunction bilateral obstruction

A

Presence of volume expansion

ANP blocks effects of renin->decreased angiotensin II therefore net result is diuresis and natiuresis

480
Q

Urinary concentration

A

Inability to absorb Na int he ascending limb and dilute the filtrate int he distal convoluted tubule, the solutes are excreted

Defective urea recycling: transporter defect reduces concentrating effect and allows urea to be excreted

481
Q

Potassium tubular dysfunction

A

Low flow luminal state and high urinary K

Small amounts of urine high K , but minimal have hyperK

Even though lot of K in urine is small opposed to what is supposed to be filtered

482
Q

Acute and chronic outlet obstruction

A

Acute-stone, one ureter

Chronic-enlarged prostate as time goes on not emptying bladder backflow reasons

483
Q

Acute bilateral ureteral obstruction

A

Increase RBF
Decrease GFR
Decrease medullary blood flow
Increased vasodilator prostaglandins, NO

Increase ureteral and tubule pressure

Increase reabsorption of Na, urea, water

Pain , azotemia, oliguria or anuria

484
Q

Chronic bilateral ureteral obstruction

A

Decrease RBF
Decrease GFR
Increase vasoconstrictor prostagladin
Increase refine

Decreasemedullary osmolarity
Decrease concentrating ability
Structural damage; parenchymal atrophy

Decrease transport functions for Na, K, H

Azotemia HTP-AVP insensitive polyuria/nature’s is, hyper Khyper Cl

485
Q

Ring picture of outlet obstruction

A

Patient with azotemia, hyper K and metabolic acidosis

486
Q

343 Harrison table 19th edition

A

Ok

487
Q

Causes of obstruction

A 
Nephrolithiasis
Strictures
Malignancy
BPH/prostate
Neurogenic bladder
Congenital
Pregnancy
488
Q

VUR

A

VU has one way valve that fails

Primary or secondary

More in male kids
Most common inherited anomaly of GU

Frequent UTI and pyelonephritis

489
Q

Kid with upper and lower infections

A

Evaluated for reflex

490
Q

Adults with voiding trouble may develop reflux that predisposes them to what

A

UTI and pyelonephritis

491
Q

BPH

A

Slow stream increase urgency
Dribble
Nocturnal
Urine forced into the ureters cause hydronephrosis

Vague pain pattern-may include low back, perineum or suprapubic area

492
Q

BPH can lead to hydronephrosis

A

Ok

493
Q

Overflow incontinence

A

Ok

494
Q

Post void residual

A

US on full and empty bladder

If >100ml indicate incomplete emptying

See overflow incontinence

495
Q

100mL urine

A

Crest pool for bacteria and infections

496
Q

Stress incontinence

A

Women child birth
Muscles of perineum lost ability to control urethra and emptying
Cough sneeze laugh too hard lose control

497
Q

What do with stress incontinence

A

Kegal sit on toilet start and stop urine stream will take time to get msucle control to stop them can do kegal anywhere

498
Q

Neurogenic bladder

A

Spinal cord trauma

Spinal myelomeningocele

Less common-spinal stenosis, herniated disc

Disruption of coordination of relaxation of sphincter during bladder contraction

As volume increases, resting pressure rises

499
Q

> 40 cm H2) increases risk of

A

Hydronephrosis and subsequent decrease in GFR

500
Q

Treat neurogenic bladder

A

Monitor as hydronephrosis may occur before irreversible injury

501
Q

Renal Lithiasis cause

A

RTA, other hormone

502
Q

Result renal lithiasis

A

Unilateral obstruction

Pain back pain radiates to groin and episodic

503
Q

Insert dye into renal lithiasis

A

See where caught

504
Q

Treat lithiasis

A

Try to pass drink a on of water and strain urine

Unable to pass-in through urethra with basket and pull through and stento to keep it open and drains hen remove stent

505
Q

Pregnancy and obstruction

A

Proximity to uterus
May persist 6 weeks post partum

First trimester-hydronephrosis in 10-15 percent

Do stent if problem but usually monitor

506
Q

Malignancy obstruction

A

Constitutional symptoms but may come in for fatigue, weight loss,

507
Q

Kidney cancer

A

Transitional CA can obstruct ureter

But can be colon, ovarian, lymphoma

508
Q

Postobstructive diuresis

A

Combo of fluid overload, urea accumulation and electrolyte imbalance

250ml/hr but can be as high as 750 ml/h

509
Q

Why get it

A

Down regulation of Na transporters during obstruction

ANP released in response to cardiac preload during obstruction

510
Q

Treat post obstructive

A

Fluid replacement in response to diuresis-75% of ruine volume and careful monitor or urine and serum osmolality as well as serum electrolytes

511
Q

58 male dysuria 8 days pain radiates back and perineum. Chills, achiness, cant start stream . Doesn’t feel like bladder is empty when finish pee.
Now small amounts of urine and spontaneous incontinence

A

Spontaneous incontinence-overflow

BPH, prostatis, UTI,

Get UA with microscopy, US, CT,

512
Q

Found he had enlarged bladder

Ureteral dilation

Hydronephrosis either unilateral or bilateral

A

Ok

513
Q

Nephrotic range proteinuria

A

Large amount of protein 3.5 g

514
Q

Nephrotic syndrome

A

Need proteinuria
Hyperlipidemia-fasting cholesterol/lipids
Hypoalbuminemia
Edema

515
Q

63 yo male polyuria polydipsia (drinking a lot) and facial swelling for 3 months.

A

Anytime patient thirsty or urinating a lot

-tip off for diabetes (losing sugar and fluid-osmotic diuretic)

516
Q

What is DM associated with

A

Nephrotic syndrome-may cause it

Hypoalbuminemia

517
Q

Why low albumin in blood stream and spilling protein in urine cause swelling

A

Lose colloid osmotic so leak out interstitial then think low so raas

518
Q

DM with edem

A

Most likely effecting kidney

519
Q

Drug decrease proteinuria

A

ACE ARB

520
Q

Type II DM

A

Annual ACR (albumen/Cr ratio)

521
Q

lupus and rheumatoid arthritis and nephrotic syndrome

A

Ok

522
Q

Infection nephrotic

A

Hep BC-cryoglobinuremia

HIV
Syphilis

Tuberculosis

523
Q

HIV

A

Focal segmental glomerulosclerisus

524
Q

Hematologic/oncologist cause of nephrotic

A

Amyloidosis
Multiple myeloma
Sickle cell
Liquid and solid tumors

525
Q

Drugs cause nephrotic

A

NSAIDS
Lithium
IV heroin

526
Q

72 year old male severe back pain for year. Works a small farm. No specific identifiable injury. He works in hostpital. Couple different physician give pain pill on separate occasion, not aware of other. Tylenol 3.

A

Hazards of opoids. Codeine is controlled. Any prescription should be done with caution.
They didn’t do PE, no chart, they just gave him pills.
Huge risk to patient and postponed care

527
Q

What else might patient take with this constellation

A

NSAIDS twice the recommended

528
Q

Effect

A

Proteinuria
-as did evaluation, did 24 hour urine to quantify and get protein electrophoresis bc his age group prone to multiple myeloma-he has indirectly transposed treatment to malignancy

529
Q

AAFP article on hematuria in adult

A

Ok

530
Q

22 yo male going to do triathlon needs physical before . Runs and does weight. He has 1+ blood

A

Hematuria in athletics

Heavy exercise induce hematuria in 80% of athletes and may have proteinuria

531
Q

Why

A

Exercising heavily, get renal ischemia for short periods of time. Result in red cells in urine. More common in swimmers, track, and lacrosse.

532
Q

Athletes have pains

A

Take NSAIDS

Also can cause hematuria

533
Q

Take home message

A

Occult hematuria always get a microscopy and a culture and sensitivity
Then re check

534
Q

Why need microscopy

A

See where cellls come from

535
Q

NSAIDS

A

Inhibit COX in kidney ibueprofin bigger offender than acetaminophen

In drug classes have variation

Net effect of renal ischemia activates RAAS*** vasoconstriction

536
Q

RAAS from NSAID

A

Up up vasoconstrict

537
Q

26 yo female ab paina fter meal better if eat tums

UA-2+ blood

A

Menstruation give false positive up to 24 hours realize starting mesntral cycle and can persist for several days after

Need UA epigastric pain? No

538
Q

Dipstick false positive

A

Up to 35% false positive

539
Q

UA how collect

A

Mid stream mid catch, wash urethra this eliminates debris around urethra that would give false information

540
Q

Myoglobin in urin

A

Give heme positive result false positive in dipstick

541
Q

Ph>9 urine, certain types of proteus infection get

A

False positive

542
Q

Vitamin C false positive

A

Can give false positive in cold a flu season can get this

543
Q

What is hematuria

A

3 RBC per high powered field

544
Q

19 yo male presents with blood in urine. Plays football was struck from right and has bruise since then urine darker than usual but has continued to play foot ball 1+ blood 2+ urobilinogen

A

Kidney protected can just observe these patients and re check in 48 to 72 hours.

Need US depending on history and physical
Falls and rapid deceleration injuries hurt kidney?

545
Q

If they are hemodynamics stable do not need a US or CT to look at kidney

A

Ok

546
Q

22 yo african American male need veal so can play college basketball . Exam normal. 6’7
2+ blood

A

Sickle cell trait

547
Q

Sickle cell trait

A

Infants screened at birth
If not causing problem then, don’t worry

Can get renal papillary necrosis and get focal segmental glomerulonephropsis-RENAL MEDULLARY CARCINOMA

548
Q

What cancer worry about with sickle cell trait

A

Renal medullary carcinoma

549
Q

What do

A

Send for UA and culture and sensitivity

550
Q

55 yo male comes for refill bp meds. Former smoker quick when given high BP 1+ blood . UA neg for blood and protein a year ago

A

Probably cancer related to smoking

551
Q

Number one risk for bladder cancer

A

Smoking

552
Q

Other question

A

How much NSAIDS

Other exposures

553
Q

Gross hematuria painless

A

CANCER until proven otherwise

554
Q

Irritation voiding symptoms with hematuria

A

Dysuria, urgency, frequency

Tips balance away from cancer-

555
Q

What could have

A

Catheter, chronic UTI, pelvic irritation, schistosomiasis

556
Q

Blood with urine

A

Also microscopy and culture and sensitivity and

Get BUN, Cr serum eval

Radiographically?

557
Q

US

A

No radiation cheaper

Less sensitive for smalls tones, small bladder mass, good for hydronephrosis!!!

558
Q

CTU

A

2 phase radiographically test sensitive for renal calculi bc done in two phases

Expensive , radiation,

559
Q

CTU. Work

A

1st scan wo contrast second with

560
Q

Cytoscopy

A

Direct visualization if sure its a lower GU how we go in to get renal stones

If stone can get with basket , can get biopsy, can cauterize active bleeding, it is invasive (risk UTI and different thought)

561
Q

US or IVP negative

A

Can go straight to cystoscopy

562
Q

RBC gone through glomerulus

A

Dysmorphic

563
Q

Rbc from down

A

Looks fine

564
Q

Chronic glomerulonephritis

A

Scarring

Cortical tubular atrophy

Interstitial inflammation

Interstitial fibrosis

Atherosclerosis

565
Q

RAAS effect

A

Vasoconstriction

Increase

566
Q

50 yo male quick smoking last week when brother died from heart attack. Works for postal service, no exercise. What are his risk factors

A

Male
Smoker (non smoker until haven’t touched for 6 months)
Diet
Obese
No exercise
2+ edema
Prolonged expiration-typical of obstructive disease
Bilateral carotid bruits
Sinus rhythm with left ventricular hypertrophy and no t wave abnormalities

567
Q

What’s wrong with this guy

A

Atherosclerosis , HTN,

568
Q

What get

A

24 hour urine and BUN, Cr, Na, 24 hour urine

569
Q

Glomerulonephritis

A

Hematuria)microscopic vs gross)

Have some degre of proteinuria

570
Q

Acute vs chronic glomerulonephritis

A

Detailed history

Renal US-chronic kidney smaller

571
Q

All nephropathy

A

Give some hematuria

572
Q

Red cell casts or sysmorphic

A

Glomerulonephritis

As few as 3-5

573
Q

Sustained proteinuria

A

> 1-2 g/24 hours

Edema and or foamy urine

574
Q

Benign proteinuria

A

Functional or transient
1-2 g/24

Fever exercise, orthostatic

575
Q

Treat

A

Low fat diet and salt reduction

Exercise lose weight

576
Q

MOA in HTN nephropathy

A

RAAS and hyperfiltration

HTN initiate RAAS and glomerulus comes under pressure with hyperfiltration from changes and fibrosis

577
Q

Hypertensive nephrosclerosis who gets

A

African americans-young

All old people

578
Q

POL1

A

In black people

579
Q

Risk factors for hypertensive nephrosclerosis

A

Smoking, HTN< low birth weight, preexisting renal injury

580
Q

Signs hypertensive nephrosclerosis

A

HTN, microhematuria and moderate proteinuria

581
Q

How control progression

A

BP

582
Q

Diabetic nephropathy

A

ECM damage changes the glomerular filtration surface makes more leaks.

583
Q

Type I vs Type 2 diabetics

A

1-changes in parallel independent of albuminuria
2-develop albuminuria without changes to nephron

Both present with edema and worsening of HTN are late findings and related to LOSS OF NEPHRONS NOT CHANGE IN GLOMERULUS

584
Q

Changes in flow

A

Ok

585
Q

Initial phase obstruction of unilateral obstruction

A

Urine backflow-increases intraluminal hydrostatic pressure

A simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR

Activation of RAAS leads to the second phase

586
Q

Second phase 6 hours

A

Decrease glomerular blood flow due to afferent arterioles vasoconstriction

587
Q

Third phase unilateral

A

Decreased luminal hydrostatic pressure and renal blood glow below baseline

588
Q

Persistence unilateral obstruction>24 hours can cause what

A

50% drop in GFR

589
Q

US

A

Solid white fluid black

590
Q

Inject dys to find obstruction

A

Dye see how dilated ureter is in unilateral obstruction

591
Q

Bilateral 2 phases

A

Initial-urine backflow-increases intraluminal hydrostatic pressure
-simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR

RAAS is activated which leads to second phase

592
Q

Second phase bilateral

A

Decrease glomerular blood flow due to afferent arterioles vasoconstriction maintains GFR

593
Q

Why just two phases

A

ANP may maintain GFR and arteriolar function

594
Q

Tubular dysfunction unilateral

A

Inability to reabsorbed sodium
Salt eating

Downregulation of receptor and anxyme activity

Have high salt regular urine from the one kidney

595
Q

Tubular dysfunction bilateral obstruction

A

Presence of volume expansion

ANP blocks effects of renin->decreased angiotensin II therefore net result is diuresis and natiuresis

596
Q

Urinary concentration

A

Inability to absorb Na int he ascending limb and dilute the filtrate int he distal convoluted tubule, the solutes are excreted

Defective urea recycling: transporter defect reduces concentrating effect and allows urea to be excreted

597
Q

Potassium tubular dysfunction

A

Low flow luminal state and high urinary K

Small amounts of urine high K , but minimal have hyperK

Even though lot of K in urine is small opposed to what is supposed to be filtered

598
Q

Acute and chronic outlet obstruction

A

Acute-stone, one ureter

Chronic-enlarged prostate as time goes on not emptying bladder backflow reasons

599
Q

Acute bilateral ureteral obstruction

A

Increase RBF
Decrease GFR
Decrease medullary blood flow
Increased vasodilator prostaglandins, NO

Increase ureteral and tubule pressure

Increase reabsorption of Na, urea, water

Pain , azotemia, oliguria or anuria

600
Q

Chronic bilateral ureteral obstruction

A

Decrease RBF
Decrease GFR
Increase vasoconstrictor prostagladin
Increase refine

Decreasemedullary osmolarity
Decrease concentrating ability
Structural damage; parenchymal atrophy

Decrease transport functions for Na, K, H

Azotemia HTP-AVP insensitive polyuria/nature’s is, hyper Khyper Cl

601
Q

Ring picture of outlet obstruction

A

Patient with azotemia, hyper K and metabolic acidosis

602
Q

343 Harrison table 19th edition

A

Ok

603
Q

Causes of obstruction

A 
Nephrolithiasis
Strictures
Malignancy
BPH/prostate
Neurogenic bladder
Congenital
Pregnancy
604
Q

VUR

A

VU has one way valve that fails

Primary or secondary

More in male kids
Most common inherited anomaly of GU

Frequent UTI and pyelonephritis

605
Q

Kid with upper and lower infections

A

Evaluated for reflex

606
Q

Adults with voiding trouble may develop reflux that predisposes them to what

A

UTI and pyelonephritis

607
Q

BPH

A

Slow stream increase urgency
Dribble
Nocturnal
Urine forced into the ureters cause hydronephrosis

Vague pain pattern-may include low back, perineum or suprapubic area

608
Q

BPH can lead to hydronephrosis

A

Ok

609
Q

Overflow incontinence

A

Ok

610
Q

Post void residual

A

US on full and empty bladder

If >100ml indicate incomplete emptying

See overflow incontinence

611
Q

100mL urine

A

Crest pool for bacteria and infections

612
Q

Stress incontinence

A

Women child birth
Muscles of perineum lost ability to control urethra and emptying
Cough sneeze laugh too hard lose control

613
Q

What do with stress incontinence

A

Kegal sit on toilet start and stop urine stream will take time to get msucle control to stop them can do kegal anywhere

614
Q

Neurogenic bladder

A

Spinal cord trauma

Spinal myelomeningocele

Less common-spinal stenosis, herniated disc

Disruption of coordination of relaxation of sphincter during bladder contraction

As volume increases, resting pressure rises

615
Q

> 40 cm H2) increases risk of

A

Hydronephrosis and subsequent decrease in GFR

616
Q

Treat neurogenic bladder

A

Monitor as hydronephrosis may occur before irreversible injury

617
Q

Renal Lithiasis cause

A

RTA, other hormone

618
Q

Result renal lithiasis

A

Unilateral obstruction

Pain back pain radiates to groin and episodic

619
Q

Insert dye into renal lithiasis

A

See where caught

620
Q

Treat lithiasis

A

Try to pass drink a on of water and strain urine

Unable to pass-in through urethra with basket and pull through and stento to keep it open and drains hen remove stent

621
Q

Pregnancy and obstruction

A

Proximity to uterus
May persist 6 weeks post partum

First trimester-hydronephrosis in 10-15 percent

Do stent if problem but usually monitor

622
Q

Malignancy obstruction

A

Constitutional symptoms but may come in for fatigue, weight loss,

623
Q

Kidney cancer

A

Transitional CA can obstruct ureter

But can be colon, ovarian, lymphoma

624
Q

Postobstructive diuresis

A

Combo of fluid overload, urea accumulation and electrolyte imbalance

250ml/hr but can be as high as 750 ml/h

625
Q

Why get it

A

Down regulation of Na transporters during obstruction

ANP released in response to cardiac preload during obstruction

626
Q

Treat post obstructive

A

Fluid replacement in response to diuresis-75% of ruine volume and careful monitor or urine and serum osmolality as well as serum electrolytes

627
Q

58 male dysuria 8 days pain radiates back and perineum. Chills, achiness, cant start stream . Doesn’t feel like bladder is empty when finish pee.
Now small amounts of urine and spontaneous incontinence

A

Spontaneous incontinence-overflow

BPH, prostatis, UTI,

Get UA with microscopy, US, CT,

628
Q

Found he had enlarged bladder

Ureteral dilation

Hydronephrosis either unilateral or bilateral

A

Ok

629
Q

Acute renal failure/acute renal injury

A

Increase Cr seen in 6 percent of hospitalized

630
Q

Treat AKI

A

Nothing proven maintain volume and stuff.

631
Q

Prerenal failure

A

Most common in host. CHF, cirrhosis, nrenovascular disease

632
Q

Intrinsic renal failure

A 
ATN
Rhabdo and ATN
Radiocontrast dyese
Emboli
TPP/HUS
Drugs
HIV/SLE
633
Q

Post Renal

A

Obstruction

Ambulatory not hospitalized

Stones, malignant, papillae-more proximal obstruction

634
Q

Intrinsic renal finding

A

HTN, GN, edema
NA retention
Hemoptysis, pulmonary hemorrhage, vasculitis,

Rbc wbc cellular casts characteristic of GN
RBC CASTS

NSAIDs-proteinuria

Allergic nephritis-eosinophils with wrights or Hansel

WBC pyelonephritis

635
Q

Post renal

A

Less ill
Delayed until azotemia is up

Fena>one 
Bland microscopic 
US is key 
Dilated Exeter calyces 
May also use furosemide renogram MAGthree
636
Q

Treat AKI

A

Support
Pre renal vol loss-IV
CHF-vasodilator or inotropy

Intrinsic-GN SLE vasculitis corticosteroids and cytotoxic
Plasma phones is-HUS
Plasma exchange-TPP
Pyelonephritis, endocarditis-antibiotics
Allergic-
Obstruction-urologist catch or stent
637
Q

What I’d nonprerenal aki progresses

A

Dialysis

638
Q

Indication dialysis

A

Volume overload refractory to diuretic agents, hyperkalemia, encephalopathy not explained, pericarditis, pleuritis, serositis, metabolic acidosis,

Provide in advance
Inability to requisite fluid for drugs

639
Q

What kind of dialysis most patients given

A

Intermittent hemodialysis

640
Q

Continuous renal replacement therapy

A

Only if IHD intolerant

641
Q

SLED

A

SLOW EFFICIENCY DIALYSIS, HYBRID TECHNIQUES MAY BE SED INSTEAD OF CRRT

642
Q

Chronic kidney disease

A

Irreversible impairment of kidney function

643
Q

More esk or CKD

A

CKD

644
Q

First step of ckd diagnosis

A

Establish chronicity

-history and prior labs and U(small kidney for chronic

645
Q

What chronic diseases have large kidney though

A

Diabetic nephropathy, HIV, multiple myeloma or amyloidosis

646
Q

Next step

A

Etiology

History, drugs disease,

PE masses , Bruit-renovascular

Electrophoresis, serum, light chains,

D< P, Ca, PTH for bone

647
Q

What labs suggest nephrotic

A

Hypoalbuminemia, hyperchlosterolemia, edema

648
Q

Uremic syndrome in CKD

A

Cr to estimate eGFR

Cr>five thirty

649
Q

Symptoms uremia

A

Anorexia, weight loss, dyspnea, fatigue, pruritis, sleep, metallic taste, confusion, encephalopathy

Hypertension, jugular distension, pleural friction rub, muscle watering, asterisks, ecchmoyses , excessive bleeding

HyperK, P, acidosis, hyperU, anemia, hypoalbuminemia, hypoCa

650
Q

Treat uremia

A

Dialysis or transplant or drug

651
Q

How treat CKD

A

Treat the HTN to slow progression
-give diuretics bc of the volume overload that causes htn

EPO-for anemia, want 90 hemoglobin

Iron supp
Restrict P eat or calcium based salt
K>6

652
Q

What potassium consider dialysis

A

Over 6 on repeat

653
Q

What big signs start dialysis

A

Anorexia, hypoalbuminemia, hyper K, weight loss

654
Q

How slow progression ckd

A

Control that htn ace arb , diuretics—-may also help control the high K

655
Q

Median wait time for transplant

A

Three to six years

656
Q

Absolute indications dialysis

A

HyperK, acidosis, encephalopathy no explained, pericarditis, serositis, uremia, failure to thrice,

657
Q

What GFR get these symptoms

A

Ten

658
Q

Does initiation of dialysis before uremic symptoms improve ESRD

A

No

659
Q

Hemodialysis

A

Brescia imino fistula

Blood pumped in and bathed

Three times a week

660
Q

Efficiency dialysis

A

Duration, blood flow rate, dialysate flow rate, surface area dialysis

661
Q

Complication hemodialysis

A

Hypotension-diabetes who’s neuropathy prevents compensatory responses (tachy vasoconstriction)

Cns

662
Q

Dialysis disequilibrium syndrome

A

Headache, confusion, from rapid solute removal early in the pts dialysis history, before adaptation to the procedure

663
Q

How avoid disequilibrium syndrome

A

Incremental induction of chronic dialysic therapy in uremic patients short durationlower flow rate

664
Q

Peritoneal dialysis

A

Don’t need circulation access.

Allows infusion of a dialysate solution into abdominal cavity across peritoneal membrane which is an artificial kidney

665
Q

Difference between PD and heme dialysi solution

A

PD must be sterile and uses lactate rather than bicarbonate

666
Q

Prob PD

A

Longer and less effective,

667
Q

But what are advantages PD

A

Independence and flexibility, gentle hemodynamics profiles

Better preservation renal function

668
Q

PD complication

A

Peritonitis -ab pain cloudy dialysate, peritoneal leukocyte count up with neutrophils
Protein loss HUGE

669
Q

Organisms of peritonitis

A

Staph aureus and staph spp gram positice
Candida

Pseudomonas

670
Q

Treatment of choice esrd

A

Transplant

671
Q

How get best transplant results

A

Living related recipient

Less ischemia and waiting time usually done prior to symptoms and better graft survival

672
Q

Graft matching

A

Improves survival

673
Q

Why is imbalance of patients and donors going to increase

A

Obesity and diabetes

674
Q

Expanded criteria donor and donors after cardiac death

A

Developed to increase dead donor kidney

675
Q

ECD kidneys-who gets

A

People who expected fare less well on dialysis

676
Q

Factors influence graft survival

A

Pretransplant blood transfusion avoid

-if encessary use leukocyte reduced irradiated blood

677
Q

Contraindications renal transplant

A

Active GNm infection, malignancy, aids, hepatitis,

678
Q

Patient should have what life expectancy to get kidney

A

Over five years

679
Q

Rejection

A

Hyperacute-presensitization

Acute-week month

680
Q

How detect rejection

A

Rise in Cr

HTN fever, reduced urine, tenderness

681
Q

How confirm rejection

A

Percutaneous renal transplant biopsy

682
Q

Treat rejection

A

Pulse of methylprednisone

Monoclonal antibody directed at human t lymphocytes

683
Q

Immunosuppressive therapy transplant

A

Three dru regimen
Calcineurin inhibitors
Cyclosporine

684
Q

Cyclosporine side effects

A

Hyper K, HTN< tremor, hirstiusm, gingival hypertrophy, gout,

685
Q

Tacrolimus

A

Hyperglycemia

Hair loss

686
Q

Prednisone

A

Steroid-

687
Q

Complication renal transplant

A

Neoplasia, infection bc of immunosuppression

Polyomavirus DNA virus BK
EPV
Non Hodgkin and squamous cell skin carcinoma

688
Q

Month one

A

CMV

Use ganciclovir

689
Q

After one month

A

Fungal pneumocystisi carinii

690
Q

Nephritic syndrome

A

Salt and water retention from reduced GFR may get circulatory congestion

RBC casts

691
Q

Proteinuria with nephrtis

A

Less than three

692
Q

Acute post strep GN

A

Positive pharyngeal skin culture
ASO titres
Hypocomplementemia

GN on biopsy

693
Q

Treat acute post strep GN

A

Correct fluid and electrolyte balance

Self limited

694
Q

Postinfections GN

A

Bacterial or viral and parasitic

Endocarditis, sepsis, hep, pneumococcal pneumonia

Feature more mild that post strep

695
Q

Post staph

A

IgA deposits IF

696
Q

Treat post infections GN

A

Control infeciton but steroids often given to avoid dialysis

697
Q

RPGN

A

GFR less than fifty percent

Complex like SLE

Pauli immune ANA

Anti GB

698
Q

SLE lupus

A

Deposit circulating immune complex

Arthralgias-butterfly skin rash, serositis, alopecia, CNS

Nephrotic diffuse GN
Active sediment, proteinuria, progressive renal insuffiency
ANA, hhypocompl, anti ds-DNA

699
Q

Treat SLE lupus

A

Glucocorticoids and cytotoxic agents
Cyclophosphamide

First bank sperm and egg before

700
Q

Pauli immune GN

A

Renal limited or systemic

PANCE, MPO, cANCA

MPO and PRthree antigens

701
Q

Treat Pauli

A

Methylprednisone and cyclophosphamide
Plasmapheresis
Pneumocystitis carnii prophylaxis

702
Q

Diagnosis henoch

A

Biopsy

703
Q

Urine spot for nephrotic

A

Yup easier

704
Q

Complications NS

A

D defiency

705
Q

MCD not respond steroids

A

Focal sclerosis

706
Q

Membranous GN

A

Sub epithelial IgG

SLE, hep B, tumors, captopril, penicillamine

707
Q

Treat membranous

A

Ace arb, prophylactic DVT

708
Q

Focal glomerulosclerosis

A

Primary acute

Secondary chronic

709
Q

MPGN

A

Ok

710
Q

Diabetic nephropathy

A

Ace arb
Glucose control

Loop diuretics is get HyperK that cant be controlled

711
Q

Asymptomatic

A

Thin basement and IgA nephropathy

712
Q

Distinguish tubulointerstitial

A

Less HTN, hematuria and proteinuria

713
Q

acute interstitial nephritis drugs

A

Increase Cr, eosinophilic rash arthralgias

Rapid if previously sensitized
Rifampin

714
Q

Tubular dysfunction lab

A

Hyper K metabolic acidosis

715
Q

How see eosinophilic

A

Hansel or wright stisan

716
Q

Systemic cause AIN

A

Leptospirosis, strep

IgG4 plasma cells

717
Q

Tubulointerstiial nephritis and uveitis syndrome

A

Weight loss, increase erythrocytes sedimentation ate

Self limited give prednisone

718
Q

Chronic interstitial nephrtis

A

Analgesic nephropathy
Asprin phenacetin

Transitional cells arcinoma

719
Q

Manifestations chronic IN

A

Papillary necrosis, calculi, sterile pyruvate, azotemia

720
Q

Chinese herbal meds

A

Severe chronic tubulointerstitial fibrosis

721
Q

Balkan endemic nephropathy

A

South east Europe

722
Q

Lithium

A

Chronic tubulointerstitial nephritis

Give valproic acid instead

723
Q

Metabolic cause of chronic IN

A

Hyper Ca with nephrocalcinosis, oxalosis, hypoK, hyperplastic Uric Emma

724
Q

Chronic IN with what systemic disease

A

Sjorgen

725
Q

Myeloma

A

Monoclonal immunoglobulin or light chain and AL amyloidosis

Filtered light chains aggregate and cause tubular obstruction, tubular damage, and inflammation

Hypercalcemia volume depletion

726
Q

Diagnose cast nephropathy

A

Light chain in urine or serum

By electrophoresis

727
Q

Dipstick negative

A

Light chain nephropathy

Positive AL amyloididid bc of proteinuria

728
Q

Diagnose ADPCK

A

Between thirty and fifty nine at least two cysts in each kidney

729
Q

ADPCK

A

HTN, normal GFR

RAAS

Give ace arb

730
Q

What is common in ADPK

A

UTI cyst infections

731
Q

RTA

A

Ok

732
Q

When get renal calculi

A

Urine supersaturated with insoluble components form low urine volume, excessive or insufficient secretion of selected compounds.

733
Q

Most stones

A

Ca based

734
Q

Ca oxalate stone

A

Hypercalcuria, hyperoxaluria

High Na diet, loop diuretic, RTA 1, primary hyperPTH, VD excess, milk alkaloids

735
Q

Hyperoxaluria

A

Malabsorption IBD, pancreatitis

736
Q

Uric acid stone

A

Chemo low pH

737
Q

Cystine stones

A

Acidic pH defect in intestinal tranpost

738
Q

Obstruction insert bladder catheter and get diuresis

A

Obstruction below bladder neck

739
Q

Insert catheter and no diuresis do US

A

Hydronephrosis obstruction above bladder neck

No hydronephrosis —low clinical suspicion—no work up, but high suspicion identify and relieve

740
Q

Hydronephrosis

A

Identify site and relieve and identify cause

741
Q

US

A

Hydronephrosis

742
Q

CT IV

A

Site of obstruction

743
Q

Tc99 MAG3

A

Renal scan to assess excretion before and after loop diuretic can assess function and difference between two kidneys

744
Q

Distinguish tubulointerstitial

A

Less HTN, hematuria and proteinuria

745
Q

acute interstitial nephritis drugs

A

Increase Cr, eosinophilic rash arthralgias

Rapid if previously sensitized
Rifampin

746
Q

Tubular dysfunction lab

A

Hyper K metabolic acidosis

747
Q

How see eosinophilic

A

Hansel or wright stisan

748
Q

Systemic cause AIN

A

Leptospirosis, strep

IgG4 plasma cells

749
Q

Tubulointerstiial nephritis and uveitis syndrome

A

Weight loss, increase erythrocytes sedimentation ate

Self limited give prednisone

750
Q

Chronic interstitial nephrtis

A

Analgesic nephropathy
Asprin phenacetin

Transitional cells arcinoma

751
Q

Manifestations chronic IN

A

Papillary necrosis, calculi, sterile pyruvate, azotemia

752
Q

Chinese herbal meds

A

Severe chronic tubulointerstitial fibrosis

753
Q

Balkan endemic nephropathy

A

South east Europe

754
Q

Lithium

A

Chronic tubulointerstitial nephritis

Give valproic acid instead

755
Q

Metabolic cause of chronic IN

A

Hyper Ca with nephrocalcinosis, oxalosis, hypoK, hyperplastic Uric Emma

756
Q

Chronic IN with what systemic disease

A

Sjorgen

757
Q

Myeloma

A

Monoclonal immunoglobulin or light chain and AL amyloidosis

Filtered light chains aggregate and cause tubular obstruction, tubular damage, and inflammation

Hypercalcemia volume depletion

758
Q

Diagnose cast nephropathy

A

Light chain in urine or serum

By electrophoresis

759
Q

Dipstick negative

A

Light chain nephropathy

Positive AL amyloididid bc of proteinuria

760
Q

Diagnose ADPCK

A

Between thirty and fifty nine at least two cysts in each kidney

761
Q

ADPCK

A

HTN, normal GFR

RAAS

Give ace arb

762
Q

What is common in ADPK

A

UTI cyst infections

763
Q

RTA

A

Ok

764
Q

When get renal calculi

A

Urine supersaturated with insoluble components form low urine volume, excessive or insufficient secretion of selected compounds.

765
Q

Most stones

A

Ca based

766
Q

Ca oxalate stone

A

Hypercalcuria, hyperoxaluria

High Na diet, loop diuretic, RTA 1, primary hyperPTH, VD excess, milk alkaloids

767
Q

Hyperoxaluria

A

Malabsorption IBD, pancreatitis

768
Q

Uric acid stone

A

Chemo low pH

769
Q

Cystine stones

A

Acidic pH defect in intestinal tranpost

770
Q

Obstruction insert bladder catheter and get diuresis

A

Obstruction below bladder neck

771
Q

Insert catheter and no diuresis do US

A

Hydronephrosis obstruction above bladder neck

No hydronephrosis —low clinical suspicion—no work up, but high suspicion identify and relieve

772
Q

Hydronephrosis

A

Identify site and relieve and identify cause

773
Q

US

A

Hydronephrosis

774
Q

CT IV

A

Site of obstruction

775
Q

Tc99 MAG3

A

Renal scan to assess excretion before and after loop diuretic can assess function and difference between two kidneys

► Med Notes (62 decks)

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