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HSS 3305 > Lecture 16 > Flashcards

Lecture 16 Flashcards

1
Q

Body Water Content

A

50-60% of body weight is water (Female-Male) found in cells, plasma and interstitial fluid

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2
Q

Electrolytes

A

Dissolved mineral salts that dissociate in solution (anions/cations)

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3
Q

What is osmoregulation controlled by?

A

Osmoregulation is controlled by water intake and excretion (sweat, urine) ie – water loss increases sodium concentration.

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4
Q

What is volume regulation controlled by?

A

Volume regulation is primarily controlled by sodium retention and excretion

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5
Q

Disturbances of H2O balance

A

Dehydration (more common) through inadequate intake and excess H2O loss (diarrhea or vomiting) or Overhydration (less common) through the excessive fluid intake when renal function is impaired

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6
Q

Hypovolemia

A

A decrease in plasma volume and loss of blood pressure

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7
Q

Regulation of Plasma pH

A

Must be maintained between 7.37 and 7.42; regulated by kidneys and respiratory system

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8
Q

What roles does the kidney play in regulating blood pH?

A
  1. Kidneys reabsorb bicarbonate and manufacture bicarbonate
  2. Acidic metabolic products are excreted by the kidney.
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9
Q

Acidosis

A

Blood pH shifts to acidic side due to an excess of H2CO3 (carbonic acid) or from a reduced amount of bicarbonate

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10
Q

Alkalosis

A

Blood pH shifts to the basic side due to a decrease of H2CO3 (carbonic acid) or from an increased amount of bicarbonate

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11
Q

Metabolic disturbance

A

Disturbance lies in bicarbonate member of the buffer pair

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12
Q

Respiratory disturbance

A

Disturbance lies in carbonic acid members of the buffer pair

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13
Q

Metabolic acidosis and compensatory mechanisms

A

Increased endogenous acid generated
Compensation: By hyperventilation to lower PCO2 and increased bicarbonate production in kidneys

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14
Q

Respiratory acidosis and compensatory mechanisms

A

Increased H2CO3 concentration - Inefficient exhalation of CO2 by lungs
Compensation: Increased bicarbonate production in kidneys

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15
Q

Metabolic alkalosis and compensatory mechanisms

A

Increased plasma bicarbonate concentration from loss of gastric juice, chloride depletion, excess corticosteroids, excess antacids
Compensation: Inefficient, requires simultaneous correction of potassium deficiency

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16
Q

Respiratory alkalosis and compensatory mechanisms

A

Reduced H2CO3 concentration due to hyperventilation
Compensation: Excretion of bicarbonate by kidneys

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17
Q

Respiratory Control of pH (increase and decrease of respiration)

A

Increased respiration lowers carbon dioxide concentration making blood more alkaline and decreased respiration causes elevation of alveolar PCO2, raising plasma carbon dioxide

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18
Q

Kidneys

A

Paired, bean-shaped excretory organs below the diaphragm adjacent to the vertebral column

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19
Q

3 basic functions of the kidney

A

Excrete waste products of food metabolism, Regulate mineral, electrolyte, acids and H2O balance, Produce erythropoietin, thrombopoietin and renin (specialized kidney cells)

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20
Q

Urea

A

End product of protein metabolism

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21
Q

Uric Acid

A

Nucleic acid metabolism

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22
Q

Erythropoietin

A

Regulates red blood cell production in marrow

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23
Q

Renin

A

Helps regulate blood pressure

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24
Q

Ureter

A

Conveys urine into bladder by peristalsis

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25
Q

Renal pelvis

A

Expanded upper portion of ureter

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26
Q

Major calyces

A

Subdivisions of renal pelvis

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27
Q

Minor calyces

A

Subdivisions of major calyces into which renal papillae discharge

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28
Q

Bladder

A

Stores urine and discharge urine into the urethra during voiding

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29
Q

Urethra

A

Conveys urine from the bladder for excretion

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30
Q

Nephrons

A

the basic structural and functional unit of the kidney using filtration, absorption and reabsorption, secretion and excretion, about 1-1.5 million nephrons in each kidney

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30
Q

The Glomerulus

A

Tuft of capillaries supplied by an afferent glomerular arteriole that recombines into an efferent glomerular arteriole with three layers of the glomerular filter

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31
Q

Mesangial cells

A

Contractile phagocytic cells that hold the capillary tuft together; regulate caliber of capillaries affecting filtration rate

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32
Q

Glomerular Filtration control Factors

A

Factors that control GFR are porosity and length of the glomerular capillary, differences in fluid pressure and oncotic pressure (inside/outside capillary) by the kidney through changes in resistance in blood flow

33
Q

What happens if there is filtration failure

A

Filtration failure will result in buildup of metabolic toxins and nitrogenous wastes (urea) in the blood (azotemia) which can lead to multi organ failure and death

34
Q

Renal tubule (proximal and distal end)

A

Reabsorbs most of the filtrate; secretes unwanted components into the tubular fluid; regulates H2O balance
Proximal end: Bowman capsule
Distal end: Empties into collecting tubules

35
Q

Control of Plasma Osmolality

A

Plasma osmolality is mainly controlled by sodium concentration and depends on water uptake and loss (diuresis [urination])

36
Q

Hyponatremia

A

Results in cell swelling

37
Q

Hypernatremia

A

Cell shrinkage (osmosis)

38
Q

Diabetes insipidus

A

Cause by lack of secretion of ADH or failure of kidney response to ADH – resulting in large amounts of urine production (20L/day) and dehydration

39
Q

Renin release

A

Released in response to decreased blood volume, low blood pressure– converts angiotensinogen to Angiotensin I

40
Q

How is Angiotensin I → angiotensin II

A

Angiotensin-converting enzyme (ACE) as blood flows through the lungs

41
Q

Hypoperfusion

A

Low blood pressure or volume –is prolonged causes renal injury

42
Q

Angiotensin II

A

Powerful vasoconstrictor (Raises blood pressure) and stimulates aldosterone secretion from the adrenal cortex (reabsorption of NaCl and H2O by kidneys)

43
Q

Diuretics, types of diuretics, and treatment

A

Increase water and sodium excretion to reduce blood volume (reduce sodium/water reabsorption)
3 main types:
Loop diuretics (furosemide) – block sodium reabsorption in ascending loop of Henle (major site of sodium reabsorption), Thaizide diuretics (hydrocholorthiazide), and Potassium sparing diuretics (spirolactone)
Treatment: hypertension, edema, CHF

44
Q

Diagnostic Evaluation of Kidney and Urinary Tract Disease

A

Urinalysis (pH, conc, glucose, protein, bile, blood, casts), Urine culture - bacteria, Blood chemistry tests, Kidney function tests, BUN (blood urea nitrogen test), Glomerular filtration rate (GFR), Creatinine clearance test, X-ray studies (with/without contrast), Ultrasound examination, Cystoscopy, Renal biopsy/histology, and CT

45
Q

Normal development of the urinary system

A

Kidneys arise from mesoderm, develop in pelvis, ascend to final position, bladder is derived from lower end of intestinal tract, ureteric buds develop excretory ducts

46
Q

Renal agenesis

A

Failure of one or both kidneys to develop (bilateral - rare, unilateral - common)

47
Q

Duplications of urinary tract

A

Complete duplication (formation of extra ureter and renal pelvis) and incomplete duplication (Only upper part of excretory system is duplicated)

48
Q

Malposition

A

One or both kidneys, associated with fusion of kidneys; horseshoe kidney; the fusion of upper pole – often of little clinical significance, may have some abnormalities in drainage of urine

49
Q

Renal Failure

A

acute (develops rapidly and tends to resolve) or chronic (develops slowly with permanent damage); is associated with retention of urea in the blood (uremia) and metabolic acidosis (inability to remove waste products)

50
Q

What does pre-renal cause?

A

Hypertension, atherosclerosis and high sugar levels from diabetes

51
Q

What does post-renal cause?

A

Often obstructive – bladder stones, prostatic diseases, cancer

52
Q

What causes Acute kidney injury?

A

Trauma/ Surgery complications (decreased renal blood flow), low BP (shock), Urinary tract blockage – stones, cancer, Medications - NSAIDS, Diseases that increase load on kidneys (toxins /muscle deterioration/hemolytic diseases)
Treatment: Treat underlying cause – if done soon enough, should prevent permanent damage to kidney – dialysis may be required until cause is treated

53
Q

Chronic kidney Injury (CKI)

A

Renal function remains regular until the number of functioning nephrons declines to 30% of normal.

54
Q

Hypertensive Nephrosclerosis

A

Complication of severe, uncontrolled hypertension, increases glomerular pressure

55
Q

Diabetic Nephropathy

A

Complication of long-standing diabetes (hyperglycemia) causing progressive impairment of renal function and protein is lost in the urine. May lead to ESRD. Once initiated, can’t be reversed but progress can be slowed dependent on glycemic control (along with Hypertension if present)

56
Q

Uremia

A

Progressive loss of renal function due to retention of excessive by-products of protein metabolism (urea) in the blood (uremia);Fluid, electrolyte, acid–base regulation failure (metabolic acidosis and anemia due to lack of erythropoietin) which causes waste accumulation in the blood

57
Q

Clinical manifestations and treatment in Uremia

A

Weakness, loss of appetite, nausea, vomiting
Anemia (failure of Epo production – endocrine function), Toxic manifestations from retained waste products (weakness, lethargy, neuropathy (delirium), cardiovascular disease, Retention of salt and water causes edema, Blood volume increased – Hypertension, Coma, convulsions, and death
Treatment: Hemodialysis, Peritoneal Dialysis, and
Transplantation

58
Q

Dialysis and its types

A

Substitutes for the functions of the kidneys by removing waste products from patient’s blood; Can be used indefinitely or during period while waiting for kidney transplant
Extracorporeal dialysis (more common): artificial kidney
Peritoneal dialysis (less common) - own peritoneum is used as the dialyzing membrane

59
Q

Renal Transplantation

A

When kidneys fail. Best if from a close relative donor (living donor -sibling match) can also be obtained from unrelated –matched deceased donor (HLA matches), More than 90% of transplanted kidneys last for 5 years with good HLA match, 10y survival rate is 50%

60
Q

Glomerulonephritis

A

Inflammation of the glomeruli caused by immune reaction within glomerulus - Autoimmunity following a beta-streptococcal infection; Could turn into ESRD without immunosuppressive therapy. Decreases urine output - waste accumulation in blood.
Diseases: Occurs in Lupus, immune complexes trapped in glomeruli and occurs in IgA nephropathy

61
Q

Poststreptococcal Glomerulonephritis

A

Occurs after infection resolved (strep throat) in affected individuals, antistreptococcal antibodies form immune complexes with strep antigens

62
Q

Anti GBM glomerulonephritis

A

Autoantibodies against basement membrane –progresses rapidly

63
Q

ANCA (anti neutrophil cytoplasmic antibody) glomerulonephritis

A

Characterized by destruction/inflammation of small blood vessels. They reach with the cytoplasmic components of neturophils

64
Q

Renal Cyst types

A

Solitary cysts common; not associated with impairment of renal function
Multiple cysts from congenital polycystic kidney disease; cysts will enlarge and destroy renal tissue which will cause early onset of kidney failure. Confirmed by ultrasound/CT

65
Q

Renal Tumor Types

A

Cortical tumors: Arise from epithelium of renal tubules
Transitional cell tumor: Arise from transitional epithelium lining urinary tract
Nephroblastoma Arise from remnant embryonic tissue: Uncommon; highly malignant, metastasizes widely; affects infants and children

66
Q

Diagnosis and treatment of renal tumors

A

Urinalysis, culture, clearance tests, Blood chemistry tests, X-ray, ultrasound, cystoscopy, biopsy
Treatment: Nephrectomy, radiotherapy, chemotherapy

67
Q

Nephrotic Syndrome

A

Glomerular renal disease associated with Marked loss of protein in the urine (nephrosis) that is caused by glomerular disease. The outcomes are the decline in protein levels in blood, edema, Ascites (fluid in abdominal cavity), and Hydrothorax (fluid in pleural cavity)

68
Q

Acute Renal Tubular Injury pathogenesis and clinical manifestations

A

Impaired renal blood flow, Tubular necrosis caused by infection, toxic drugs or chemicals, Any condition associated with shock and marked drop in BP – decreased blood supply and damage to tubules
Clinical manifestation: Acute renal failure: Oliguria, anuria

69
Q

Urinary Tract (UTI)

A

Very common; may be acute or chronic, Most infections are caused by gram-negative intestinal bacteria that contaminate perianal and genital areas and ascend urethra

70
Q

How to prevent a UTI

A

Free urine flow
Large urine volume
Complete bladder emptying
Acid urine: Most bacteria grow poorly in an acidic environment

71
Q

Cystitis

A

Affects only the bladder More common in women than men; urethra in female is shorter; in young, sexually active women - sexual intercourse promotes transfer of bacteria from urethra to bladder
(Pain during urination, desire to pee frequently, bacteria and leukocytes in urine, can spread upwards into renal pelvis and kidneys)

72
Q

Pyelonephritis + symptoms

A

Ascending infection from the bladder (ascending pyelonephritis) and Carried to the kidneys from the bloodstream (hematogenous pyelonephritis); frequently associated with cystitis
Symptoms: localized pain and tenderness over affected kidney

73
Q

Vesicoureteral Reflux (VUR)

A

Failure of valve allows bladder urine to reflux into ureter and into kidneys in severe cases – valve defect/ neurogenic/ urethra blockage causing UTIs, bladder problems, kidney infection and scarring in severe cases

74
Q

Urinary Calculi

A

Stones may form anywhere in the kidney/urinary tract. If they remain in the urinary tract they can grow larger

75
Q

Urinary Calculi predisposing factors

A

Low fluid intake, High concentration of salts in urine saturates urine, Urinary tract infections and obstructions

76
Q

Staghorn calculus and treatment

A

Urinary stones that increase in size to form large branching structures that adapt to the contour of the pelvis and calyces
Treatment
Cystoscopy: remove stones lodged in distal ureter
Xray/shock wave lithotripsy: Stones lodged in proximal ureter are broken into fragments that are readily excreted

77
Q

Urinary Obstruction, complications, diagnosis, and treatment

A

Blockage of urine outflow leads to progressive dilatation of urinary tract proximal to obstruction, eventually causes compression, destruction of kidney parenchyma and atrophy; can be bilateral or unilateral
Complications: stone formation, infections, Kidney damage/failure
Diagnosis and treatment: Pyelogram (X-ray with IV contrast – collects in urine, CT scan)

78
Q

Kidney cancer

A

Typically form in the tubules (renal cell carcinoma) most are found before they can spread, easily treated when caught early causes hematuria, fatigue, weight loss, and anemia

79
Q

Bladder/ureteral cancer types

A

Urothelial carcinoma (most common) - cells that line the bladder/ureters and squamous and adenocarcinoma (rare) causing hematuria, painful/frequent urination, and lower back pain on 1 side

80
Q

Urethral cancer + symptoms

A

Rare – 1% of all urogenital cancers
Symptoms: Hematuria, painful urination, unable to empty bladder – frequent urge to urinate

HSS 3305 (21 decks)

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