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PATHO > EXAMS 3 > Flashcards

EXAMS 3 Flashcards

1
Q

function of the kidney (vitamin D)

A
  • homeostasis (electrolytes and water)

- excretion (urea, electrolytes and water)

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2
Q

production of kidney / target of kidney

A

PRODUCTION

erythropoietin
angiotensin

TARGET
aldosterone
ADH

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3
Q

vitamin d kidney

A

increases calcium absorption from the gastrointestinal tract

regulates calcium deposition in bone

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4
Q

causes of urinary tract obstruction

A
  • developmental defects
  • calculi (stones)
  • pregnancy
  • benign prostatic hyperplasia
  • scar tissue resulting from infection and inflammation
  • tumors
    neurological disorders such as spinal cord
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5
Q

damaging effects of urinary obstruction

A

stasis of urine = predisposes to infection and stone formation

development of backpressure = interferes with renal blood flow and destroys kidney tissue

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6
Q

manifestations of urinary obstruction

A

DEPENDS on

- site, cause and rapidity in which condition develops

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7
Q

COMMIN SYMPTOMS OF URINARY OBSTRUCTION

A
  • pain
  • sign and symptoms of UTI
  • manifestations of renal dysfunctions
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8
Q

definition of kidney stones

A
  • crystalline structures that form from components of urine
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9
Q

requirements for formation of KIDNEY STONE

A
  • urinary environment that supports continued crystallization of stone components
  • concentration of stone components in the urine
  • ability of stone components to complex and form stones
  • the presence of substances that inhibits stone formation
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10
Q

types of kidney stones

A
  • calcium stones ( oxalate or phosphate ) = HARD SINGLE BROWN
  • magnesium ammonium phosphate stones( stag horn) = SMOOTH ROUND WHITE
  • uric acid stones = MULTIPLE YELLOWISH, RADIOLUSCENT
  • cystine stones = seen in cystinuria RADIO OPAQUE DUE TO SULPHUR
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11
Q

kidney stone treatment PREVENTATIVE

A

diet restriction
calcium salt supplementation
thiazide
cellulose phosphate

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12
Q

general kidney stones treatment

A

preventative
treatment for pain
removing stones
antibiotic for infection

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13
Q

removing stones kidney stone

A

ureteroscopic removal
percutaneous removal
extracorporeal lithotripsy

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14
Q

diagnosis of kidney stones

A

urinalysis
radiography
intravenous pyelography
ultrasonography

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15
Q

types of UTI

A

asymptomatic bacteriuria
symptomatic infections
lower UTIs - cystitis
upper UTIs - pyelonephritis

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16
Q

uncomplicated UTIs

A

E. coli

staphylococcus saprophytic

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17
Q

complicated UTI

A

gram positive cocci

S.aureus, group B streptococcus

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18
Q

diagnosis and treatment of UTIs

A

diagnosis based on symptoms and examination of the urine for prescience of micro organisms

  • x ray file, ultrasonography, CT and renal scans are used to identify contributing factors
  • urine dipstick
  • TREATMENT OF ITI IS BASED ON THE PATHOGEN CAUSING THE INFECTION
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19
Q

causes of glomerulonephritis

A

disease that provoke a proliferation inflammation of the endothelial, mesangial, epithelia cells of the glomeruli

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20
Q

inflammatory process of glomerulonephritis

A
  • damages the capillary wall
  • permits red blood cells to escape into the urine
  • produces hemodynamic changes that decrease the GFR
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21
Q

immune mechanisms of glomerulonephritis

A

glomerular antibodies

circulating antigen antibody complexes

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22
Q

characteristics of glomerulonephritis

A
  • hematuria with red cell casts
  • a diminished glomerular filtration rate (GFR)
  • azotemia (presence of nitrogenous wastes in the blood)
  • Oliguria
  • hypertension
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23
Q

proximal tubular disorder

A

affects bicarbonate reabssorption

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24
Q

distal tubular defects

A

affect the secretion of fixed metabolic acids

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25
Q

peritoneal dialysis

A

removes nitrogenous waste products such as excess fluid and electrolyte from the blood by means or peritoneal membrane

APPROX 10-15% patients are receiving peritoneal dialysis

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26
Q

hemodialysis

A
  • removes nitrogenous waste products excess fluids and electrolytes from the blood by the means of ARTIFICIAL KIDNEY

APPROX 90% of all dialysis patients receives hemodialysis

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27
Q

renal failure

A

a condition in which kidneys fails to remove metabolic end products from the blood and regulate the fluid, electrolytes, and pH balance of the extracellular fluids

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28
Q

underlying causes of renal failure

A
  • renal disease
  • systemic disease
  • urologic defects of nonrenal origin
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29
Q

prevention and early diagnosis of active renal failure

A
  • those with pre existing renal insufficiency and diabetes

- elderly persons due to the effects of aging on renal reserve

30
Q

ACUTE RENAL FAILURE

A
  • abrupt in onset

- often reversible if recognized early and treated appropriately

31
Q

CHRONIC RENAL FAILURE

A
  • end result of irreparable damage to the kidneys

- develops slowly, usually over the course of a number of years

32
Q

CAUSES OF ACUTE RENAL FAILURE (PRERENAL)

A
  • hypovolemja
  • decreased vascular filling
  • heart failure and cardiogenic shock
  • decreased renal perfusion due to vasoactive mediators, drugs, diagnostic agents
33
Q

causes of acute renal failure (POSTRENAL)

A

bilateral ureteral obstruction

bladder outlet obstruction

34
Q

COMMON CAUSES OF CHRONIC RENAL DISEASE

A 
hypertension 
diabetes mellitus
polycystic kidney disease 
obstructions of the urinary tract 
glomerulonephritis
cancers
autoimmune disorders 
diseases of the heart or lungs 
chronic use of pain medication
35
Q

medical management treatment of renal failure

A
  • dialysis ( hemo and peritoneal )
  • transplantation

DIETARY MANAGEMENT

  • protein
  • carbohydrates, fat, calories
  • potassium
  • sodium and fluid intake
36
Q

common causes of neurogenic bladder

A
  • stroke and advanced age
  • parkinson’s disease
  • spinal cord injury
  • injury to the sacral cord or spinal roots
  • radical pelvic surgery
  • diabetic neuropathies
  • multiple sclerosis
37
Q

spastic bladder dysfunction (neurogenic bladder)

A
  • failure to store urine
  • neurologic lesions above the sacral cord allow neurons in the micturition center to function reflexively without control from the CNS centers
38
Q

flaccid bladder dysfunction

A
  • bladder emptying is impaired
  • neurologic disorders affect motor neurons in the sacral cord or peripheral nerves that control destrusor muscles contraction and bladder emptying
39
Q

goals of treatment neurogenic bladder disorders

A
  • prevent bladder overdistention, UTI, life threatening renal damage
  • reduce the undesirable social and psychological effects of the disorder
40
Q

treatments for neurogenic bladder disorders

A
  • catheterization
  • bladder retraining
  • pharm manipulation
  • surgical procedures
41
Q

stress incontinence

A
  • involuntary loss of urine during coughing laughing sneezing or lifting
42
Q

urge incontinence

A

involuntary loss of urine associated with a strong desire to void (urgency)

43
Q

overflow incontinence

A

involuntary loss of urine that occurs with intravesicular pressure exceeds the maximal urethral pressure because of bladder distraction in the absence of detrusor activity

MIXED INCONTINENCE = combination and urge incontinence

44
Q

what is shock

A

tissues are not adequately perfused, causes general widespread impairment of cellular metabolism ( glucose and oxygen )

45
Q

factors of shocks

A

defective heart function
blood volume changes
metabolic or toxic changes

46
Q

manifestations of shock

A
  • include hypotension
  • tachycardia
  • increased respiratory rate
47
Q

circulatory failure shock (hypoperfusion of organs)

A

acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate resulting in cellular hypoxia

48
Q

risk factors of multiple organ dysfunction syndrome (MODS)

A

sepsis, prolonged periods of hypotension, hepatic dysfunction, infarcted bowel, advanced aged, severe trauma, alcohol abuse

49
Q

causes of multiple organ dysfunction syndrome (MODS)

A

most common: sepsis, septic shock

other (severe injury, trauma, burns, major surgery)

50
Q

manifestations of MODS

A 
respiratory
hepatic 
renal
GI
myocordial failure
51
Q

TREATMENR OF multiple organ dysfunction syndrome (MODS)

A
  • respiratory system: mechanical ventilation
  • GI system: enteral feeding or hyperalimnetation (increase calories for hypermetabolic state)
  • renal system ( dialysis or continuous help filtration for fluid and electrolyte balance
    cardiovascular- intro pic drugs or vasopressors
52
Q

cardiogenic shock

A

inability of the heart to pump adequate blood to meet body’s demands

CAUSES: MI mysocaridal comtusion, sustained arrhythmias, cardiac surgery

CLINICAL MANIFESTATIONS: cardiac output

53
Q

hypovolemic shock

A

insufficient intravascular fluid
- occurs with acute loss of 15 or 20% of circulating blood volume

MANIFESTATIONS : thirst, increased HR, cool and clammy skin, decreased arterial blood pressure, decreased urine output, changes in mentation, poor skin tugor

54
Q

distributive or vasodilatory shock

A

loss of BLOOD VESSEL TONE, enlarged vascular compartment, displacement of vascular volume away from the heart and central circulation

3 shock that share the basic circulatory pattern of distributive shock = neurogenic, anaphylactic, septic shock

55
Q

neurogenic shock ( distributive )

A
  • caused by decreased sympathies control of blood vessel tone, sympathetic outflow to the blood vessels

RARE AND USUALLY TRANSITORY

56
Q

anaphylactic shock

A

severe reactions

warm/burning sensation of the skin, itching l, choking, wheezing, chest tightness, dyspnea

TREATMENT: remove the trigger, administer oxygen, antihistamine, corticosteroids, epinephrine ( EpiPen)

57
Q

Sepsis

A

suspected or proven infection, plus a systemic inflammatory response ( FEVER TACHYCARDIA, TACHYPNEA, elevated WBC altered mental state hyperglycemia IN THE ABSENSE IF DIABETES

58
Q

treatment of sepsis

A
  • airway management to treat hypoxenua
  • early administration of fluids within the first 3 hours
  • broad spectrum antibiotic PRIORITY TREATMENT
  • central venous access is recommended for IV fluids, medications, frequent blood draws
59
Q

septic shock

A

most common type of vasodilatory shock associated with sever infection and the systemic response to infection

60
Q

MANIFESTATIONS of septic shock

A
  • HYPOtension and warm, flushed skin
  • fever and increased leukocytes are present
  • an elevated serum lactate or metabolic acidosis
61
Q

obstructive shock

A

circulatory shock that results from mechanical obstruction of the flow of blood through the central circulation

62
Q

causes of obstructive shock

A
  • dissecting aortic aneurysms, cardia tamponade, pneumothorax, atrial myxoma, and evisceration of abdominal contents into the thoracic cavity

TREATMENT: pulmonary embolectomy, pericardiocentesis or the insertion of a chest tube for correction of a tension pneumothorax or hemothorax

63
Q

COMPLICATIONS OF SHOCK

A
  • pulmonary injury
  • acute renal failure
  • gastrointestinal ulceration
  • disseminated intravascular coagulation (DIC)
  • multiple organ dysfunction syndrome (MODS)
64
Q

parkinson’s disease

A

a degenerative disorder of basal ganglia function and results in variable combinations of tremor, rigid, bradykinesia

CHARACTERISTICS: destruct nigrostriatal pathway, reduction in striata concentration of DOPAMINE

65
Q

myasthenia gravis (NEUROMUSCULAR JUMCTIOMS)

A

disorder of transmission at the neuromuscular junction THAT AFFECT THE COMMUNICATION BETWEEN MOTONEURON AND INNERVATED MUSCLE CELL

CAUSE: cashed by antibody mediated LOSS OF ACH in the neuromuscular junction

66
Q

multiple sclerosis ( EXACERBATIONS AND REMISSIONS OVER MANY YEARS IN SEVERAL DIFFERENT SITES CNS)

A

demyelinating disease of the CNS
- most common non traumatic cause of neurologic disability among young and middle aged adults

INITIAL: normal or near normal between neurologic functions between exacerbations

As the disease progresses, there’s less improvement between exacerbations and increasing neurologic dysfunction

67
Q

AMYOTROPHIC LATERAL SCLEROSIS (ALS)

A

devastating neurologic disorder that SELECTIVELY AFFECTS MOTOR FUNCTION

disease typically follows a progressive course with a mean survival period of 2-5 years from the onset of symptoms

68
Q

dawn phenomenon

A
  • early morning glucose elevation WITHOUT nocturnal hypoglycemia
  • related to nocturnal growth hormone elevation
    TREATMENT: alter timing and dose of insulin
69
Q

somogyi effect ( TYPE 1 DM )

A

most common in type 1 DM and in children

  • hypoglycemia with rebound hyperglycemia
  • counter regulatory hormones in GLUCONEOGENESIS
70
Q

inflammatory bowel disease ( ulcerative colitis, chrons disease)

A

chrons disease: can affect anywhere ( patches )
- recurrent granulomatous type of inflammation that can affect anywhere from mouth to anus )

ulcerative colitis: nonspecific and continuos of the colon

71
Q

chronic stable ANGINA

A
  • associated with a fixed coronary obstruction DISPARITY BETWEEN CORONARY BLOOD FLOW AND METABOLIC DEMANDS OF THE MYOCARDIUM

CAUSES

  • atherosclerotic plaque disruption
  • platelet aggregation
72
Q

cushing syndrome

A

excess cortisol level

PATHO (6 decks)

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