Exam 4

Question 1

What is hypoxic drive and why is it important to understand this concept?

Answer 1

Usually, the drive to breathe is caused by an increase in Carbon Dioxide (CO2) levels, but in patients with chronic lung diseases, they have chronically high levels of CO2. The CO2 receptor that stimulayes breathing is used to the elevated CO2 and will no longer drive breathing. Drop in O2 becomes main breathing trigger.

If individual is using O2 to breathe you must keep O2 sat below normal 85-90%, so that they are hypoxic (lowo2) to drive breathing. If you bring O2 up, they will stop breathing.

Question 2

What is paroxysmal nocturnal dyspnea?

Answer 2

Paroxysmal nocturnal dyspnea is a sudden acute dyspnea,
episode of shortness of breath that occurs at night, often waking the pt from sleep.
-occurs in patients w/ left sided heart failure
-results from pulmonary edema

Question 3

What are general signs and symptoms of lung disorders and how does the body compensate?

Answer 3

General S/S
fatigue, lethargy, muscle weakness, acid-base imbalance

Compensates by:
-TACHYCARDIA to increase HR
-CHRONIC HYPOXIA , increases erythropoietin (produce rbc) and can cause secondary polycythemia. To decrease risk of 2polythemia, keep O2 sats low.

Question 4

Explain the concept of ventilation perfusion matching and its importance.

Answer 4

ventilation is the amount of air entering/leaving alveoli
perfusion is the amount of blood that flows to alveoli

this ratio should be equal (1).
more vent, less perfusion -> dead space, pulmonary embolism

less vent, more perfusion -> atelectasis, shunt

Question 5

What is meant by anatomical dead space, physiological dead space, and alveolar dead space? Which would increase in a patient with pneumonia?

Answer 5

Anatomical Dead Space: regions of the respiratory tract due to anatomy, but no gas exchange occurs. (=0 healthy person)

Alveolar Dead Space: alveoli that should be involved in gas exchange but are not due to a disease.
-vol. of inhaled air delivered to alveoli that receives no blood flow.
-caused by PULMONARY EMBOLISM or HYPERINFLATION OF ALVEOLI (PEEP/COPD)

Physiological Dead Space: Anatomic DS + Alveolar DS
-increases in pt w/ pneumonia

Question 6

Know the age range of patients who suffer from rhinoviruses.

Answer 6

occur in early fall and late spring in people between the ages of 5-40

Question 7

Know the age range of patients who suffer from parainfluenza viruses.

Answer 7

occur in children younger than 3

Question 8

Know the age range of patients who suffer from respiratory syncytial virus (RSV)

Answer 8

occur in winter and spring in children younger than 3

Question 9

Know the age range of patients who suffer from coronaviruses and adenoviruses.

Answer 9

Coronaviruses and adenoviruses can affect all age groups,

Question 10

Understand the development and progression of Pneumococcal Pneumonia.

Answer 10

Pneumococcal pneumonia develops when Streptococcus pneumoniae infects the lungs, causing inflammation (malaise, chills/fever, crackle sounds) in alveoli. Serious exudate forms, and you will have a productive cough.

The serous exudate will turn into fibrous/purulent exudate. Since it is an infection, it will have pus. (consolidation). When you cough you may rupture blood vessels so it will be blood-tinged sputum w/pleuritic pain.

WBC go to alveoli and denature hemoglobin, liquify exudate (reabsorbed into circulation), phagocytizing and removing pathogen from alveoli. When this happens, you have resolution

Question 11

What bacteria causes TB?

Answer 11

Myobacterium Tuberculosis hominis

Question 12

As it relates to TB, what is the difference between a primary infection, secondary infection, latent TB, and miliary TB? Which ones will test positive on a TB test, which ones are contagious?

Answer 12

Primary TB: After inhaling TB bacteria, macrophages begin a cell-mediated immune response, leading to a Ghon focus containing macrophages and T cells. The bacteria are usually isolated in the Ghon foci and are inactive and not contagious. A positive TB test typically develops 3 to 6 weeks after the initial infection

Latent TB: inactive/alive TB bacteria are contained within the Ghon foci. Individuals with latent TB test positive, not contagious.
-if reactivates at subsequent date it becomes secondary TB

Secondary TB: have latent TB, already have been exposed to TB. Reinfection from inhaled droplet nuclei. Reactivation of previously healed primary lesion. Now immunocompromised at later date and develop an active infection. positive TB test, contagious, pathogen in sputum
-bacteria and IS damage tissues and create cavities.

-signs of chronic pneumonia; gradual destruction of lung tissue
-low grade fever, night sweats, anorexia, weight loss, sputum purulent, pathogen in sputum

Miliary TB: This occurs from progressive primary TB leads to bacteria eroding blood vessels and spread through the body. Miliary TB lesions look like grains of millet in the tissues (found in muscle/milk)

+TESTS: primary, latent, secondary
contagious: 2ndary tb, miliary

Question 13

What are some signs and symptoms of TB?

Answer 13

low-grade fever, night sweats, anorexia and weight loss, and sputum that becomes purulent and often contains blood

Question 14

What are the signs and symptoms of asthma, the difference between intrinsic and extrinsic asthma, and their triggers?

Answer 14

S/S:
-productive cough, marked dyspnea, tight feeling in chest, agitation, wheezing, thick mucus, rapid breathing, accessory muscle use, tachycardia

Intrinsic asthma/nonatopic is triggered by non-allergic factors, triggered by respiratory infection, cold, exercise, drugs

(topic) Extrinsic: caused by allergens, trigger type 1 hypersensitivity reactions- IgE mediated

Question 15

How is asthma treated?

Answer 15

◦
1) avoid trigger factors.
Medications include inhalers (bronchodilators, such as albuterol)
glucocorticoids/ leukotriene antagonists (to reduce inflammation)

all above treat acute attacks

Cromolyn sodium (a prophylactic medication that inhibits release of substances from sensitized mast cells and decreases hypersensitivity, but has no value during acute attacks, since mast cells already released histamine

Question 16

Understand the early vs late phase response in asthma and the signs and symptoms.

Answer 16

Extrinsic asthma has an early phase response (10 to 20 minutes) and a late phase response (4 to 8 hours).

s/s
bronchoconstriction
inflammation w/edema
increased secretion of thick mucus

Question 17

What is the difference between wheezing and stridor and what do they indicate?

Answer 17

Wheezing indicates obstruction. It is associated with intrathoracic airway (lower airway) obstruction and characterized by prolonged expiration with wheezing.
Rib cage retractions as ribs pull inward but air doesn’t leave lungs

stridor as associated with extra thoracic airway (upper airway) obstruction, leading to impairment of inspiration and inspiratory stridor.
High pitched sound heard while inhaling
Inspiratory retractions as ribs moved outward and body wall expand with ribcage

Question 18

What is a Ghon Focus and a Ghon complex? In what patients will you see them and how are they formed?

Answer 18

A Ghon focus is a granulomatous lesion containing macrophages and T cells that forms in the lung during initial TB infection.

A Ghon complex consists of nodules in lung tissue and lymph nodes.
-caseous necrosis inside the nodules
calcium may deposit in the fatty area of necrosis, making it visible on x-rays.

Ghon complexes are seen in patients with primary TB infection. They are formed as part of the body’s cell-mediated immune response to the inhaled Mycobacterium tuberculosis bacteria

Question 19

What is typical and atypical pneumonia; signs and symptoms of each?

Answer 19

Typical pneumonia: bacterial pneumonia
involves bacteria in the alveoli.
It can be lobar (affecting an entire lobe) or cause bronchopneumonia (patchy distribution over more than one lobe).

It is characterized by inflammation and purulent exudate, and a productive cough. Pneumococcal pneumonia is the most common bacterial pneumonia

Atypical Pneumonia: viral pneumonia
viral infections of the alveolar septum or interstitium.

-unproductive cough (dry and hacking), lack of consolidation,
decreased lung defenses predisposing to bacterial infection.
fever, headache, and muscle aches

Question 20

What is pleural effusion, what are the different types, and how is it diagnosed? treated?

Answer 20

Pleural effusion is the accumulation of fluid in the pleural cavity. The different types are hydrothorax, empyema, chylothorax, and hemothorax. Diagnosed by XRAY and ultrasound. Treated by thoracentesis and treat based on cause.

Question 21

Hydrothorax

Answer 21

accumulation of serous fluid, seen in heart failure, renal failure and liver failure.
-yellowish fluid

Question 22

Empyema

Answer 22

infection in the pleural cavity with pus, signifying infection.
-pus has debris from dead cells, proteins and leukocytes

Question 23

Chylothorax

Answer 23

ruptured lymphatic vessel, milky white, results from trauma and inflammation

Question 24

Hemothorax

Answer 24

blood in the pleural cavity
-chest injury/surgery
-requires drainage via thoracentesis

Question 25

Why is pleural effusion dangerous?

Answer 25

Too much fluid in the parietal cavity can cause a separation of the visceral and parietal pleura to separate and the lungs will collapse (atelectasis)

Question 26

How does pleural effusion differ from pulmonary edema?

Answer 26

Pleural effusion is the accumulation of fluid in the pleural cavity, which is the space between the parietal and visceral pleura surrounding the lungs. -left heart failure Pulmonary edema is the accumulation of fluid in the alveoli. -right heart failure

Question 27

What is a pneumothorax? Name the different types of pneumothoraxes.

Answer 27

Air enters the pleural cavity, separating visceral and parietal pleura. Air takes up space and restricts lung expansion. Partial/complete collapse of the lung include spontaneous, [traumatic] -tension -open

Question 28

Spontaneous/closed Pneumothorax

Answer 28

Air filled blister/bleb on the lung ruptures, air enters and separates pleura. (Atelectasis) Air moves into pleural space and ruptured bleb is sealed off. -primary - no disease -secondary - underlying disease present -No affect on unaffected lung with inspiration and expiration

Question 29

Open Pneumothorax

Answer 29

hole or opening in the chest wall (often from trauma), and air enters pleural cavity through the wound on inhalation and leaves on exhalation. -The heart shifts towards the unaffected lung during inflation (mediastinal flutter), impairs venous return -Shifts back to affected lung during exhalation -decreases the amount of air entering the unaffected lung during inspiration (unaffected can't inflate properly)

Question 30

Tension Pneumothorax

Answer 30

Most dangerous air enters pleural cavity through wound on inhalation, cannot leave on exhalation, so more and more air accumulates in the pleural cavity, compression of unaffected lung, mediastinum shifts to opposite side (unaffected lung), inferior vena cava gets compressed, venous return impaired significantly & CO reduced

Question 31

S/S of pneumothorax, diagnosis, treatment

Answer 31

increased RR ipsilateral lung pain (pain on side where lung collapsed) Asymmetry of chest during inspiration decreased breathing sounds on affected side Diagnosis xray, CT, ultrasound Treatment put in chest tube, remove air, v+p pleura come back, close wound small spontaneous -> air is reabsorbed on its own needle aspiration or closed drain system

Question 32

What are the different types of COPD, results in?

Answer 32

COPD: group of chronic respiratory disorders resulting in progressive tissue destruction and obstruction of the air passages. Can result in respiratory failure caused by severe hypoxia. May result in cor pulmonale (R sided heart failure due to lung disease) -chronic bronchitis -emphysema

Question 33

Emphysema? S/S? Etiology?

Answer 33

Breakdown of alveoli wall, aveoli lose their elasticity because of an increase in elastase, due to migration of Eosinophils and Neutrophils in lungs. Normally what neutralizes elastase is alpha 1 tripson, but w/ increase in elastase, not enough inhibitor. Begins to break down alveolar wall. Fusion of different alveolar sacs. This loss of elasticity makes it easy to get air into lungs, but hard to get out. Loss of pulmonary capillaries. Loss of elastic fibers. Etiology/cause -Exposure to air pollutants -Smoking or genetic. Neutrophils in the alveoli secrete elastase. Increased neutrophils due to inhaling irritants, increase in elastase, damage alveoli by breaking down elastic tissue. Elastase decrease antitrypsin. Genetic: antitrypsin deficiency S/S Dyspnea Hyperventilation w/prolonged expiratory phase Anorexia Clubbed fingers w/secondary polycythemia Breathing w/pursed lips

Question 34

Chronic Bronchitis? Etiology/cause? Characteristics S/S?

Answer 34

Inflammation of the bronchi from cigarette smoke -obstruction of small airways -Changes in bronchi due to constant irritation from smoking/exposure to industrial pollution. -Effects are irreversible and progressive Characteristics: inflammation, obstruction, repeated infection, chronic coughing, increased number of mucus cells, hypersecretion of mucus, chronic, productive cough s/s constant productive cough shortness of breath mucus secretions thick and purulent cough more severe in morning bc mucus builds overnight airway obstruction, hypoxia, cyanosis

Question 35

What is a DVT, what is the major concern regarding a DVT, and how is it treated?

Answer 35

A DVT is a deep vein thrombosis. The major concern is the risk of pulmonary embolism. Treatment includes TPA/ thrombolytic agent.

Question 36

Explain the pathophysiology of an asthma attack.

Answer 36

Asthma: Periodic episodes of severe, but reversible airway inflammation. Seen in people w/hypersensitive airways. -bronchospasm (smooth muscle around airway contracts and narrows) -mucus hypersecretion, further blocking airway -Airway edema (swelling) due to being inflamed. -epithelial cells get injured -airflow limitation -frequent/severe acute asthma attacks can cause permanent damage to lungs.

Question 37

Describe the pathophysiology of cystic fibrosis, its cause, diagnosis and signs and symptoms.

Answer 37

it is a genetic disorder that is autosomal recessive. Person must inherit one copy from each parent to inherit the gene. Mutation in CTFR gene that regulates amount of Cl and Na. -Defective chloride channel -> high NaCl in sweat -Respiratory mucus is low in Nacl and water, develop thick mucus, resulting in airway obstruction, respiratory tract is blocked, and reproductive tract is blocked. Causes: genetic autosomal recessive carriers are asymptomatic family history -> get genetically tested diagnosis- sweat analysis, stool analysis for fat and trypsin content, pancreatic enzymes, DNA test, pulmonary function test to check extent of damage S/S salty skin malabsorption w/steatorrhea (bulky, fat, foul odor stool) abdomen distended failure to gain weight chronic cough, frequent resp. infections hypoxia, fatigue, exercise intolerance barrel chest (chest overinflated due to air trapping)

Question 38

Know the organ systems affected in patients with cystic fibrosis and the signs and symptoms associated.

Answer 38

primarily affects the respiratory and digestive systems, reproductive systems. -Lungs/Pancreas Lungs: mucus obstructs airflow. Unable to get air into/out of lungs, air gets trapped (atelectasis), increased risk of infection, respiratory failure, or cor pulmonale (R sided heart failure due to increased pressure in lungs) Pancreas: digestive enzymes unable to reach small intestine. Pancreatic ducts are blocked and materials back up into the pancreas, causing inflammation, resulting in pancreatitis. Since enzymes can't reach duodenum, they aren't digesting what they eat and are suffering w/malabsorption and malnutrition. -Diabetes mellitus (beta cells make insulin, destroyed) -bile/pancreatic ducts blocked first signs in newborn where SI gets blocked by mucus. They have a bowel obstruction and fail to pass meconium (first stool), tarry.

Question 39

What is Cor Pulmonale and how does it develop?

Answer 39

Cor Pulmonale is right heart failure due to lung disease, developing from chronic hypoxia and pulmonary hypertension.

Question 40

Why do patients with cystic fibrosis develop diabetes mellitus?

Answer 40

Thick mucus blocks pancreatic ducts, damaging the beta cells in the pancreas. Beta cells are responsible for producing insulin, which helps regulate blood sugar. Damage to beta cells leads to insulin deficiency, causing high blood sugar and diabetes.

Question 41

What is infant respiratory distress syndrome, what is the cause, and who are most at risk?

Answer 41

-Seen in premature neonates born before type 2 alveolar cells are turned on. These cells produce surfactant. Premature infants born not producing enough surfactant will have difficulty inflating lungs. -lack of surfactant, infants can't inflate their alveoli. -protein-rich fluid leaks back into alveoli and blocks oxygen uptake further.

Question 42

Why are patients with COPD more likely to develop polycythemia?

Answer 42

Patients with COPD often experience chronic hypoxia. This chronic hypoxia can lead to an increase in erythropoietin, which in turn can cause secondary polycythemia (too many rbc)

Question 43

What are the different types of incontinence?

Answer 43

Stress incontinence: increased intra-abdominal pressure forcing urine through external sphincter (laugh,cry,sneeze) Urge incontinence: overactive bladder, invol. loss of urine associated w/strong desire to void Mixed: stress + urge Overflow incontinence: urine loss when bladder pressure exceeds maximum urethral pressure, absent muscle contraction. You don't feel need to pee, but as pressure builds, urine leaks. Nocturnal enuresis: bed wetting Postmicturition dribble: urine remaining in urethra after voiding slowly leaks out after urination Continuous urinary leakage: constant leaks of urine due to an inherited abnormality or sphincter (valve) injury. No bladder control Functional Incontinence: a physical/mental impairment keeps you from making it to the toilet in time.

Question 44

What are the different types of diuretics and how do they work?

Answer 44

Diuretics remove excess water by the kidneys. They are used to treat HTN, pulmonary edema, and congestive heart failure [Potassium Wasting] Hydrochlorothiazide/Lasix. -mild diuretics, monitor K+, cardiac dysthymias. othostatic HTN Furosemide -potent diuretic [Potassium Sparing] Spironolactone -aldosterone antagonist-Aldosterone is a hormone that promotes sodium and water retention by the kidneys and increases potassium excretion. Osmotic diruetic -given IV, Osmotic diuretics are filtered by the kidneys, but they aren't reabsorbed. -increase osmotic pressure in the kidneys, which pulls water into the tubules, leading to more urine being produced and fluid loss from the body.

Question 45

What will happen to GFR if you dilate/constrict afferent/efferent arteriole?

Answer 45

AFFERENT arteriole: Dilation: increase GFR Constriction: decrease GFR EFFERENT arteriole: Dilation: decrease GFR Constriction: increase GFR

Question 46

Explain the pathophysiology of post streptococcal glomerular nephritis; what type of hypersensitivity reaction is this?

Answer 46

It's a kidney infection that develops 7-10 days post streptococcal infection. -Type III hypersensitivity reaction the antigen-antibody complex is deposited into the glomerular capillary wall, results in glomerular inflammation. Increased capillary wall permeability

Question 47

What are some signs and symptoms of post streptococcal glomerular nephritis?

Answer 47

flank pain due to swelling of kidneys urine dark (cola) due to hematuria, cloudy (proteinuria) -erythrocyte casts (skeleton remaining of cell after internal contents removed) -decreased urine production as GFR declines (oliguria) -azotemia (increased BUN & Creatinine) -Edema, retaining salt and water, loss of protein -increased BP due to decreased GFR and increased renin

Question 48

What is cystitis, its causes, and what are its signs and symptoms?

Answer 48

Caused by bladder wall and urethra inflamed, red and swollen, may be ulcerated. Bladder capacity is reduced. Lower abdominal pain, Localized s/s -dysuria (pain/burn when pee) -frequency and urgency as inflamed bladder is irritated by urine Systemic s/s fever, general malaise, nausea, leukocytosis

Question 49

What is the difference between cystitis and pyelonephritis?

Answer 49

Cystitis is bladder inflammation and lower uti, pyelonephritis is kidney inflammation and upper uti

Question 50

What is the pathophysiology, cause, signs and symptoms of pyelonephritis?

Answer 50

One or both of the kidneys involved. Infection involving the ureter, renal pelvis, and medullary tissue. -caused by E. coli, purulent exudate fills kidney pelvis and medullary tubules inflamed w/necrosis. -if severe, compresses the renal artery and vein and obstruct urine flow S/S -urinary casts consisting of leukocytes/renal epithelia. cells -dull, aching pain in the lower back, resulting from stretching of the renal capsule -chills w/mod-high fever

Question 51

What are the different types of kidney stones and what causes these different types to be formed?

Answer 51

Types of kidney stones include calcium, struvite, uric acid, and cystine stones. Calcium stones - oxalate/phosphate (Most Common) -spinach Struvite (Mg Ammonium Phosphate) - bladder infections -softest stone Uric stones - too high uric acid -gouty arthritis Cystine stones - AA cystine, hardest of all stones

Question 52

What measures might a person prone to developing kidneys stones take to decrease their risk of developing stones?

Answer 52

stay hydrated, eat fewer oxylate rich foods

Question 53

What is one treatment for ALL kidney stones?

Answer 53

increase fluid intake, lithotripsy (high energy sound waves to break stone into smaller pieces)

Question 54

How does a kidney stone damage the kidney?

Answer 54

A kidney stone can obstruct urine flow, cause infection, kidney damage. postrenal

Question 55

What is acute renal injury and what are some causes and signs and symptoms?

Answer 55

Sudden decrease in kidney function. Prerenal -blood supply is decreased by shock, dehydration, or vasoconstriction Postrenal - urine flow is blocked -stones, tumors, enlarged prostate Intrinsic - kidney tubule function decreased -ischemia, toxins, intratubular obstruction.

Question 56

What is the pathophysiology, causes, signs and symptoms, and treatment of acute tubular necrosis?

Answer 56

Intrarenal injury of tubular cells. Caused by destruction (ischemia, nephrotoxic drugs (contrast, gentamicin) Obstruction (sepsis, myoglobin- muscle severely damaged release myoglobin and blocks renal tubule) Renal tubule can recover if agent is removed, damaged cells removed, and tubular cells get regenerated. Put pt on diuretic, flush out blockage, if successfully flushed, cells that make up renal tubule can repopulate. Treat: identify the cause, use diuretics, dialysis

Question 57

What are the different phases of acute renal injury and how do you know if a person is in the recovery phase?

Answer 57

[Initiation phase] Lasts several hours to days from event to tubular injury -initial damage done to kidney [Maintenance phase] -person goes from producing urine to not producing urine (nonoliguric - oliguric) -decrease GFR, retain metabolic wastes, fluid retention, edema [Recovery phase] repair of renal tubule -gradual increase in urine formation -creatinine drop -diuresis despite increased metabolic wastes How to know if pt moved from maintenance to recovery phase? -pt has diuresis, increased urine production

Question 58

Pt most susceptible to acute renal injury

Answer 58

diabetics, pt w/renal insufficiency, pt on nephrotoxic drugs, elderly, pt on NSAID, pt who had XRAY contrast

Question 59

What electrolyte imbalances would you expect to see in a patient in kidney failure; how are they treated?

Answer 59

Hyponatremia (↓ Sodium) – Diluted due to fluid retention; treat with fluid restriction or dialysis. Hyperphosphatemia (↑ Phosphate) – Kidneys can't excrete it; treat with phosphate binders, diet change, dialysis. Hypermagnesemia (↑ Magnesium) – Reduced excretion; avoid Mg meds, give calcium, dialysis if severe. Hypocalcemia (↓ Calcium) – Binds with phosphate; treat with calcium supplements, vitamin D, phosphate control. Hyperkalemia (↑ Potassium) – Dangerous arrhythmias; treat with insulin+glucose, calcium gluconate, binders, dialysis. Metabolic acidosis (↑ H+) – Kidneys can't remove acid; treat with bicarbonate, dialysis.

Question 60

Describe the different types of renal dialysis; what are the benefits and risks/side effects of each?

Answer 60

Peritoneal dialysis - done at home w/peritoneal membranes, need entry in abdominal cavity -main complication is abdominal infection, can lead to peritonitis -you would know pt has peritonitis if you remove fluid from abd. cavity and it has a strong odor, cloudy, signifying infection Hemodialysis - done at hemodialysis unit, need entry point in vein/artery (av fistula) shunt may be clogged or infected blood vessel used for shunt becomes damaged and a new site must be selected required 3x a week, 4hrs (time consuming) in between sessions, metabolic waste builds up

Question 61

Who is at the greatest risk of developing a UTI?

Answer 61

females more susceptible than men due to shorter urethra males w/prostatic hypertrophy, benign prostatic hyperplasia (cant fully empty bladder) pregnancy

Question 62

What is creatinine and BUN and how are they used clinically?

Answer 62

Creatinine is the best indicator of renal function. You have to lose 75% of kidney function before creatinine rises. BUN- blood urea nitrogen measure amount of nitrogen in blood if kidney fail, they can't remove waste from blood

Question 63

What are some complications and signs and symptoms of chronic renal failure?

Answer 63

CKD: gradual irreversible damage to kidney and it is progressive, fewer functioning nephrons, decreased GFR for more than 3 months remaining nephrons must filter more and hypertrophy before any s/s - 75% function lost Altered neuromuscular junction (fatigue, peripheral neuropathy, restless leg syndrome, uremic state -increased metabolic wastes) GI issues - anorexia, nausea WBC/Immune dysfunction - impaired platelet function, uremic bleeding, uremic frost (lose urea in sweat and its white and dusty)

Question 64

List the stages of chronic renal failure and the characteristics of each.

Answer 64

Stage 1: Kidney damage w/ normal or increased GFR -GFR > or = 90. no changes in blood val Stage 2: Kidney damage w/mild increase in GFR -GFR 60-89, no s/s bc not 75% yet no changes in blood val Stage 3: Moderate decrease in GFR -increase in creatinine and K+ GFR 30-59 Stage 4: Severe decrease in GFR (15-29) -prep pt for dialysis Stage 5: Kidney failure GFR <15 -pt on dialysis/kidney transplant

Question 65

Why might an elderly patient have normal creatinine levels but a reduced GFR?

Answer 65

Elderly patients may have reduced muscle mass, decreased renal function, compensatory mechanisms mask decline in function, meds, hydration.

Question 66

Explain the pathophysiological process of osteodystrophy seen in patients with chronic renal failure.

Answer 66

Hyperphosphatemia occurs because the kidneys can’t excrete it. Hypocalcemia happens because phosphate binds to calcium. Increased PTH is released to raise calcium, causing bone resorption (calcium taken from bones). Metastatic Calcifications can occur when calcium and phosphate combine and deposit in soft tissues. Decreased Vitamin D Activation reduces calcium absorption from the gut, leading to more PTH release. Impaired Osteoblasts (bone-building cells) means less bone formation, leading to bone loss.

Question 67

What is nephrotic syndrome and what are some signs and symptoms?

Answer 67

basement membrane of glomerular cells affected. Seen in individuals' w/infections. -significant proteinuria -plasma protein levels drop causes: lupus, diabetes, infection s/s hypoprotinemia decreased plasma oncotic pressure edema hyperlipidemia

Question 68

How does nephrotic syndrome differ from nephritic syndrome?

Answer 68

Nephritic syndrome is when the glomerular is affected and nephrotic is when basement membrane of glomerular cells are affected.

Question 69

What is the difference between a lower and upper urinary tract obstruction; which one affects both kidneys, which one only affects one kidney?

Answer 69

Lower urinary tract obstruction Below ureterovesical junction bilateral Upper urinary tract obstruction Above ureterovesical junction unilateral

Question 70

What is hydronephrosis and its causes; how does hydronephrosis damage the kidney?

Answer 70

Hydronephrosis is the swelling of a kidney due to urine buildup, caused by obstruction, damaging kidney tissue -usually happens in 1 kidney -increased pressure inside renal capsule -compartment syndrome compresses blood vessels in kidney, leading to ischemia -stasis of urine (infection risk)

Question 71

What type of renal cancer is seen in children; what is the cause of it?

Answer 71

Wilms tumor is the most common renal cancer in children due to abnormal tumor suppressor gene.

Question 72

What is the difference between a simple cyst and polycystic kidney disease; what are the signs and symptoms of each?

Answer 72

Simple cyst epithelial cavities fill w/fluid very common, acquired over time, everyone develops eventually, can be symptomatic/asymptomatic usually no s/s, flank pain, hematuria, infection, HTN -do not affect kidney function or destroy internal architecture of kidney PKD genetic (autosomal dom-adults) (auto recess- children) more agressive in children by 12-13 need kidney transplant no s/s until 30-50s

Question 73

What is the cause of osteodystrophy associated with chronic renal failure and what hormone(s) is/are activated?

Answer 73

Osteodystrophy is caused by imbalances in calcium and phosphate due to renal failure, with parathyroid hormone being activated.

Question 74

What is the difference in adult vs juvenile polycystic kidney disease?

Answer 74

Adult: autosomal dominant, no s/s until 30-50s Children: autosomal recessive, more aggressive, by 12-13 need transplant

Question 75

What is urinary retention and how is it diagnosed?

Answer 75

Urinary retention is the inability to empty the bladder -damage at sacral level/after anesthesia -micturition reflex blocked -failure to void diagnose by assessing bladder function, observe how frequent peeing, hesitancy to urinate, weak or interrupted stream, post void residual volume gives info abt patient ability to empty bladder

Question 76

What's the best way to determine how much a patient is retaining?

Answer 76

catheterizing them to see how much volume is left post void.