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AA. Patho 2 > Urinary System Disorder > Flashcards

Urinary System Disorder Flashcards

1
Q

force of gravity, which is always pressing water out from the blood vessel is called?

A

hydrostatic pressure

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2
Q

osmotic pressure is maintained by?

A

inside the blood vessel there is 50% electrolytes/sodium, and 50% albumins. the albumins come from Liver to blood and they are preserved by the KD (which prevents it from letting it out through the glomeruous)

  • either LR or KD pathology, can cause an imbalance of albumin in blood compartment and change status quo
  • this causes changes in oncotic pressure - partial or total edema depending on how serious LR is damaged
  • if albumin level is in trouble bc KD can’t guard it, it can cause edema
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3
Q

where is KD located?

A

retroperitineally

between level T12 and L3

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4
Q

Urinary Tract infections may involve?

A

urethra, prostate, bladder, or/and kidney (pyelonephritis)

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5
Q

the urinary tract, from Kidney to urethral meatus is normally?

A

sterile, and resistance to bacterial invasion

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6
Q

the major defense against infections in urinary tract is?

A
  • urine acidity
  • complete emptying of bladder during urination (micturition)
  • competent sphincters (urethral and uretero-vesical)
  • mucosal immune barrier
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7
Q

almost all cases of UTI are associated with?

only 4- 5% of UTI are of what kinds?

A

most are associated with ascending infection from urethra up to the urinary bladder and the kidney

few are of hematogenous spread as systemic infection

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8
Q

in uncomplicated cases of UTI, what is affected

A

only urethra is affects, resulting in urethritis

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9
Q

in more complex cases of UTI what is affect?

A

cystitis (ascended infection of urinary bladder), and pyelonephritis (infection ascended to Kidney and affected everything but glomerulus

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10
Q

what are some risk factors of complicated UTIs?

A
  • immuno-compromised individuals
  • elderly
  • pregnancy (any, even uncomplicated UTI during pregnancy is to be treated/monitored in hospital)
  • obstruction to urinary flow (calculi, benign or malignant prostate growth, anatomically abnormal ureter, neurologically caused obstruction)
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11
Q

the most common UTI etiology is?

A

Gastrointesteinal is most common

  • E.coli
  • klebsiella
  • enterobacteriae
  • staphylococcus aureus
  • STD (N. gonorrheae)
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12
Q

what are clinical presentations of UTI?

A

urinary frequency
urgency
dysuria
lower abdominal and flank pain
uretheral discharge (mostly males)
systemic symptoms (fever, nausea, vomiting, chills) if infection is systemic with the kidney involvement (pyelonephritis)
-UTI may be asymptomatic as well (esp elderly)
-in GI cause of UTI, there is presence of leukyocytes esterase in urine

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13
Q

how are UTI diagnosed?

A

-bacteria in urine, collected by clean-catch technique or catheterization
-urethral swab and culture (if STD is suspected)
-in complicated UTIs (pyelonephritis, systemic infections): CBC, electrolytes, BUN, creatinine, and blood cultures are required
=differential diagnosis includes all disorders, presented with abdominal/pelvic discomfort

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14
Q

what are S&S of pyelonephritis?

A

infection in ascending KD - so flank or costovertebral pain, fever, malaise, body aches (flu-like symptoms with flank pain), not necessarily systemic but it can be

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15
Q

what is Red Flag fro UTIs?

A

UTI during pregnancy

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16
Q

how do you tx UTI?

A
  • typically antibiotics [antibiotic prophylaxis in “stubborn” cases]
  • but in asymptomatic bacteruria in elderly, diabetics, or patients with indwelling catheters should not be treated with antibiotics
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17
Q

what are some preventive measures for UTI?

A
  • voiding after intercourse
  • complete voiding
  • prevention of KD stones
  • TX of benign prostatic hypertrophy / hyperplasia
  • cranberry juice
  • avoid using diaphragm as contraceptive device who suffered more than 3 UTIs per year
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18
Q

what is Renal Cell Carcinoma (RCC)?

A

most common renal cancer

- it originates from glandular renal epithelium (adenocarcinoma) in 95% of cases

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19
Q

what are risk factors of renal cell carcinoma?

A

smoking
obesity
excessive use of phenacetin
acquired cystic kidney disease in dialysis patients
ADPKD
exposure to radiopaque contrast dyes during nuclear medicine test
asbestos exposure
cadmium exposure
leather tanning and petroleum products exposure
some cases are familia syndromes

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20
Q

what are S&S of Renal Cell Carcinoma?

A
  • usually do not appear until late
  • hematuria (this is why either gross or microscopic blood in urine are considered RED FLAG for immediate medical referral)
  • flank pain
  • fever of unclear origin
  • palpable mass (at times)
  • polycythemia and hypertension
  • hypercalcemia
  • ectopic secretion of endocrine hormones: paraneoplastic syndrome
21
Q

Renal Cell Carcinoma is second most common cancer (after Oat Cell Cancer in LU) that has….?

A

paraneoplastic syndrome - which is ectopic secretion of endocrine hormones (renin and erythopoietin)

22
Q

what are some cancers that metastasize to bone more readily?

A

cancers of KIDNEY, LU, prostate, thyroid, breast, multiple myloma, malignant myloma

23
Q

Renal Cell Cancer is diagnosed by?

A
  • abdominal imaging (CT, US, MRI)
  • clinical finding
  • confirmation and grading: needle biopsy
  • staging: chest x-rays, LV function tests, CT scan of the chest and abdomen/pelvis, bone scan
24
Q

what are tx options for Renal Cell Carcinoma?

A

partial or extensive KD ectomy, radiation, immunotherapy for some

[chemotherapy is not considered effective]

25
Q

Bladder Cancer usually originates from?

A

transitional epithelium of urinary bladder (urothelium) - this is the most delicate transitional epithelium of the whole human body

26
Q

what is the 4th most common cancer in males? and in which population?

A

Bladder Cancer

most common among white population

27
Q

what genetic factor is associated with progression of Bladder Cancer?

A

deletion of p53 gene

28
Q

what are risk factors for Urinary Bladder Cancer?

A

smoking
phenacetin abuse (analgesic abuse)
chemotherapy due to another malignancy (cyclophosphamide)
chronic cystitis, caused by a tropical helmint shistosoma hematobium
UB stones
industrial chemicals exposure (rubber, dyes, dry cleaners, electric cable and textile industries)

29
Q

what are Symptoms and signs of Urinary Bladder Cancer>

A

-most patients will present with asymptomatic hematuria before systemic symptoms

other possible presentations:
anemia
dysuria
burning upon urination
urgency and frequency of micturition
pus in urine (pyruia)
pelvic pain
pelvic mass
30
Q

how is Urinary Bladder Cancer diagnosed?

A

by clinical suspicion
ultrasonography
cystoscopy
confirmed by biopsy

31
Q

what are differential dx of Urinary Bladder Cancer?

A

same as KD cancer - all abdominal and pelvic disorders, including masses

32
Q

what is the most common cause of acute renal failure?

A

acute tubular necrosis (ATN)

33
Q

what are major causes of Acute Tubular Necrosis?

A
  1. ischemia, due to myocardic infarction or hypovolmic shock (no blood coming to KD); tubules of KD are very sensitive to blood supply
  2. nephrotoxic drugs and chemicals (antimicrobial drugs, organic solvents, pesticides, myoglobin, heavy metals as mercury, lead, gold compounds)
34
Q

what is pathogenesis of Acute Tubular Necrosis?

A

ischemia or toxins cause tubular damage with inability to secrete and reabsorb filtrate of glomeruli

as a response, glomeruli cease to filter and constrict

increased glomerular pressure leads to leakage of plasma and collapse of tubules by compression (interstitial edema)

tubules disabled –> glomeruli disabled –> tubules compressed –> the outcome could be either massive tubular necrosis with anuria or reverse to normal functions

*when KD stops concentrating urine, the space outside of tubules is saturated and tubules collapses and become necrotic

35
Q

what is clinical presentation of Acute Tubular Necrosis?

A

initial phase: first 36 hours, precipitating event occurs (toxin damage)

oliguric phase: ~10 subsequent days; decreased urinary output, uremia, fluid overload, electrolyte imbalance. these events can lead to severe arrhythmias, brain edema, GIT disturbances

diuretic phase: gradual increase in urine volume but still with inability to concentrate and reabsorb ultra-filtrate of plasma. this is very dangerous stage as well, and may lead to development of secondary infections

Recovery phase: usually 3rd week; improving concentration ability of kidney, normalization of creatinine and BUN, restoration of tubular function.

36
Q

what is Glomerular Disease / Glomerulonephritis?

A

mostly auto-immune inflammation of glomeruli

37
Q

what is etiology of Glomerulonephritis?

A

as any auto-immune, loss of tolerance of immune system to self tissues due to prior exposures to viral, bacterial antigens or connective tissues disorders with obscure etiology
-post streptococcal glomerulonephritis is common example

38
Q

what is pathogenesis of Glomerulonephritis?

A

once immune system reacted on streptococcal invasion, it is then perpetuating response by targeting glomerular membranes by immuno-globulins designed to kill bacteria initially.
as a result, glomerular membranes )fenestration and basement membranes) appear to be damaged and blood components are leaking creating a chaos in blood metabolism
- you get rusty urine, red casts of RBC

39
Q

what are clinical syndromes of glomerulonephritis? - NEPHRITIC SYNDROME

A
  • partial edema
  • -mild albumin ratio
  • skin rashes

mostly due to damage of fenestration membranes of glomeruli
presents with hematuria, hypertension, slight proteinuria, periorbital edema, petechial skin (bc it is vasculitis, it not only affects KD, you also have immune reaction against many capillaries for skin, torso) hemorrhages, fever, flank pain, and malaise
if post-streptococcal, usually occurs 2-3 weeks after either strep throat or (most commonly) impetigo (strep skin infection)

40
Q

what are clinical syndromes of glomerulonephritis? - NEPHROTIC SYNDROME

A
  • massive albumin in uria
  • total edema, so swollen unrecognizable

mainly due to further massive damage of both fenestration and basement membranes of glomeruli.
most common causes are food allergies in children, drug toxicities, blood cancers
accompanied by massive leakage of albumins (proteinuria), generalized edema, hyperlipidemia, loss of albumins in blood compartment (hypoalbuminemia)

41
Q

what is normal pH of blood?

A

7.35 ———– 7.45

acidosis – alkalosis

42
Q

alkaline blood

A

if blood is slightly alkaline, it would NOT be easy for oxygen to attach to hemoglobin; which means there is loss of affinity of hemoglobin to oxygen

43
Q

it blood is acidic?

A

there is higher affinity of hemoglobin to attach to oxygen, but hemoglobin becomes too greedy and keeps the oxygen for itself

44
Q

what organs help blood maintain pH?

A

LU and KD axis
LU exhale volatile acid, which is carbonic acid

KD clears fixed acid, KD produces hydrogen ion and re-absorb bicarbonate acids (base acids)
[metabolism produces sulfuric acids, hydrochloric acids, lactic acids bc we are active)

*if LU can’t descend, then KD grasp more
If KD can’t do its job, LU hyperventilates; LU is trying to help KD

45
Q

what is respiratory acidosis (measured by arterial blood analysis)?

A

blood becomes more acidic bc respiration is inadequate, LU do not descend or exhale volatile acid, mostly chronic, KD will reabsorb bicarbonate to protect what LU cannot do

46
Q

what is metabolic acidosis (measured by arterial blood analysis)?

A

improper metabolism - ketone bodies are acid, people who secrete too much hydrochloric acids in competitive sports, KD words hard by loosing hydrogen and reabsorbing bicarbonate; LU tries to help KD so people hyperventilate, to at least get rid of volatile acids

47
Q

what is respiratory alkalosis (measured by arterial blood analysis)?

A

hyperventilation, high altitude bc atmospheric pressure is changing, people who have anxiety

48
Q

what is metabolic alkalosis (measured by arterial blood analysis)?

A

persistent vomiting bc acid in ST and once you exuberantly vomit you become alkaline

breathing becomes shallow, bc LU doesn’t want to help you get rid of acids anymore, bc you just got rid of them

49
Q

respiratory acidosis, metabolic acidosis, respiratory alkalosis, metabolic alkalosis contribute to what conditions?

A

hypoxia and metabolic reactions

AA. Patho 2 (8 decks)

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