Exam 4 part 3 Flashcards

1
Q

bronchiectasis

A

widening of the bronchial tubes that allows mucus buildup

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2
Q

asthma pathophysiology

A

bronchi and bronchioles are excessively responsive to stimuli leading to bronchoconstriction, inflammation with edema, and increased secretion of thick mucus –> interfere with air flow

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3
Q

cystic fibrosis pathophysiology

A
  • Genetic disorder: Autosomal recessive
  • Defective chloride channel -> high NaCl in sweat
  • Less Na+ and water in respiratory mucus and in pancreatic secretions - Mucus is thicker
  • Obstructs airways
  • Obstructs the pancreatic and biliary ducts
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4
Q

cystic fibrosis etiology

A

Genetic disorder: autosomal recessive
Carriers are asympotmatic
Family history –> genetic testing

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5
Q

cystic fibrosis s/s

A
  • salty skin
  • malabsorption with steatorrhea (bulky, fatty, foul stools)
  • abdominal distension
    failure to gain weight
  • pulmonary involvement –> chronic cough, frequent respiratory infections
  • as lung damage proceeds –> hypoxia, fatigue, exercise intolerance
    chest may be overinflated due to air trapping (barrel chest)
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6
Q

cystic fibrosis primary effects on organs

A

Lungs and pancreas
- Obstruct passages
Lungs: mucus obstructs air flow
- causing air trapping or atelectasis
- Increase risk of infection
- Respiratory failure or cor pulmonale
Pancreas: digestive enzymes unable to reach small intestine.
- Ducts of exocrine pancreas become blocked
- pancreatitis
- Malabsorption / malnutrition
- Diabetes Mellitus
Blockage of bile duct by mucus
First signs appear in new born in which small intestine become blocked by mucus

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7
Q

cor pulmonale

A

right sided heart failure due to pulmonary HTN (by COPD and cystic fibrosis)

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8
Q

diabetes in CF patients

A

build up of mucus in pancreas damages insulin producing cells

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9
Q

respiratory distress syndrome

A
  • lack of surfactant, alveoli can’t inflate
  • protein rich fluid leaks into alveoli and blocks o2 intake
  • preterm infants most at risk
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10
Q

COPD and polycythemia

A

decreased o2 in the blood causes more RBCs to be made (erythropoeitin)

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11
Q

nocturnal enuresis

A

bed wetting

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12
Q

Postmicturition dribble

A

urine remaining in the urethraafter voiding the bladderslowly leaks out after urination

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13
Q

Continuous urinary leakage

A

constant leakage of urine due to an inherited abnormality or sphincter (valve) injury
(no bladder control)

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14
Q

Functional incontinence

A

A physical or mental impairment keeps you from making it to the toilet in time.
- brain damage, neurological impairment or spinal injury
(interferes with voluntary neurological control of the bladder)

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15
Q

diuretics function

A

remove excess water by the kidneys (not used if renal disease present) - dilute urine
- HTN
- CHF
- pulmonary edema

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16
Q

hydrochlorothiazide

A

mild diuretic - K wasting (can cause arrythmias)

17
Q

furosemide (lasix)

A

potent diuretic - k wasting (can cause arrythmias)

18
Q

spironolactone

A

k sparing diuretic
- aldosterone antagonist
(can cause arrythmias)

19
Q

osmotic diuretic

20
Q

side effects of k wasting diuretics

A

excessive loss of electrolytes - muscle weakness, cardiac arrythmias, orthostatic hypotension

21
Q

What will happen to GFR if you dilate/constrict afferent(enter)/efferent(exit) arteriole

A

Dilating afferent arteriole and constricting efferent arteriole increases GFR.
constricting afferent arteriole and dilating efferent arteriole decreases GFR.

22
Q

pathophysiology of post streptococcal glomerular nephritis

A
  • Proliferative inflammatory response
  • develops around 7-10 following streptococcal infection (group A beta-hemolytic Streptococcus - associated with strep bacteria)
23
Q

post streptococcal glomerular nephritis hypersensitivity

A

type 3
the antibody-antigen complex are deposited in the glomerular capillary wall or extravascular tissue - activation of complement, increased capillary wall permeability

24
Q

s/s streptococcal glomerular nephritis

A
  • flank pain due to swelling of kidneys
  • urine - dark (cola colored) and cloudy
    – Proteinuria
    – Hematuria
    – Erythrocyte casts (skeleton of what remains of a cell after the insides have been removed)
  • decreased urine production as GFR declines –> oliguria
    – Azotemia (presence of nitrogenous wastes in the blood)
    – Edema due to sodium and water retention, also loss of protein
  • increased BP due to decreased GFR and increased renin
25
Q

cystitis

A
  • lower UTI
  • bladder inflammation and infection
  • caused by urinary retension
  • dysuria, smaller bladder, systemic signs of infection, lower ab pain, blood coming from bladder wall