Patho Exam 3


When infection reaches the kidneys; potentially organ/life threatening. Usually caused by urinary tract obstruction; females 5 times more likely to develop.

ARDS (acute respiratory distress syndrome)

Occurs when fluid builds up in alveoli and prevents lungs from filling with oxygen.

Asthma (Reactive airway disease)

Chronic inflammatory disorder of the airway; can occur from any airborne irritants; leads to inflammation, wheezing, and constricted airways


Incomplete expansion of part of the lungs

Chronic bronchitis

Respiratory disease (lasting at least 3 mo/year) in which mucus membranes in the bronchial passages become inflamed.

COPD (chronic obstructive pulmonary disease)

Group of lung diseases that block airflow and make breathing difficult. (Emphysema, chronic bronchitis, asthma, and CF all fall under COPD)

Cystic fibrosis

Autosomal recessive gene trait causes thickening of CT leads to fibrosis. Exocrine glands secrete abnormally thick mucus d/t defective epithelial ion transport. Thick mucus causes obstruction of bronchioles and predispose lungs to infection.


Permanent damage to lung(s); ^CO2
Min. cyanosis
Purse lip breathing
Hyperresonacnce on chest percusion
Barrel chest
Exertional dyspnea
Prolonged expiratory time
Speaks in short jerky sentences
Uses accessory muscles to breathe


bloody sputum (usually w/ cough)

Lung cancer

Uncontrolled growth of abnormal cells in one or both lungs. Cells do not function normally in the exhange of O2 and CO2. It is the top cause of cancer deaths in men and women


Difficulty breathing while lying down

Pleural edema

Buildup of fluid in interstitial tissue (in the lungs)

Pleural effusion

Fluid buildup in pleural space (between ribs and lungs)

Early R.A.T. is late to B.E.D (respiratory distress s/s)

Early sx: Restlessness
Late sx: Bradycardia
Extreme restlessness
Dyspnea (severe)

Small-cell lung cancer

(AKA oat cell cancer)
Makes up 10-15% of lung cancers
highly malignant (brain metastasis is common)

Tripod position

Indication of respiratory distress

Tuberculosis (TB)

Infects macrophages that attack and consume TB. Will see Ghon Complexes on CXR


If air flow is disrupted it is a ventilation problem


If blood flow is disrupted, it is a perfusion problem

What (s/s) would you see if cancer metastasized to the brain or spinal cord?

Impaired neuro/motor function; LOC

What is the difference between atelectasis and pneumothorax? What are the

Atelectasis: incomplete expansion of alveoli (part of lung)
Pneumothorax: air in pleural space causing pressure on lung preventing expansion

What is the difference between an OPEN pneumothorax and a TENSION Pneumothorax? Which is most dangerous?

Open pneumothorax: occurs when air accumulates between chest wall and lung
Tension pneumothorax: when air is trapped in the pleural cavity resulting in increased pressure and mediastinal shift (most dangerous).

What is the significance of tracheal deviation (mediastinal shift)?

The trachea is displaced to the side w/ less pressure, meaning there is an increase in pressure caused by a tension pneumothorax

What is the definition of Hypercapnia and what can cause it?

Too much CO2 in the blood
Caused by problem w/ ventilation

What does the abbreviation "TCDB" stand for and why is this done?

Turn, cough, deep breath: helps to keep alveoli open and prevent further collapse

What does PaO2 measure and what is the normal range?

Measures oxygen in the blood (hypoxemia), nl range 80-100mmHg

What is a pneumothorax?

Air in the pleural space, as a result of the air in the pleural space, there is a partial or complete collapse of the lung.

What is hypoxia; how is hypoxia measured; and what is the normal range?

Hypoxia is low oxygen in the tissue, measured by SaO2, >95%

What is the precipitating even of ARDS and, what is one long-term effect?

Sepsis (other causes; lung/mult trauma, shock)
Long term effect: permanent lung damage, and psychological and cognitive impairment d/t lack of O2

What three factors cause atelectasis?

Blockage of air passages (bronchus/bronchioles)
Pressure on the outside of the lung
Surfactant failure

What is the 1st indicator of hypoxia?


A patient has been receiving 100% oxygen therapy by way of a nonrebreather mask for several days. He reports tingling in his fingers and shortness of breath. He is extremely restless and states that he has pain beneath his breastbone. Based on this histor

A. Hypercapnia resulting from decreased carbon dioxide elimination
B. Oxygen-induced atelectasis
C. Pleural effusion
D. Increased pH

What test is used to determine PaO2?

Arterial blood gas (ABG)

What does SaO2 measure?

Measures tissue perfusion (hypoxia). >95%

What causes a pneumothorax?

Trauma to chest: GSW/knife wound, rib fracture, some medical procedures. (Can also occur spontaneously)

6 P's of Dyspnea

Pulmonary/bronchial constriction
Possible foreign body
Pump failure

Causes of hemoptysis

TB (most common)
Mycobacterial infections (destroy pulm tissue)
Acute/Chronic bronchitis

Indicators of severe hypoxia

Tripod position
Use of accessory muscles

TB s/s; tx; dx

S/S: Progressive fatigue/Malaise
Pleuritic chest pain
Low grade temp (late afternoon)
Anorexia/Wt loss
Night sweats
Tx: 9 mo abx course (usually INH w/ B6)
Decreased activity
Isolation until neg sputum
TB skin test/quantiferon gold

Acute Tubular Necrosis (ATN)

Damage to kidney tubules: kidneys will suffer permanent damage (death) if enough tubules die.
most common in hospitalized pts

ADH (antidiuertic hormone)

Secreted by posterior pituitary gland; excretion caused by low blood volume, low sodium and high osmolarity of body fluids (ADH causes fluid retention to relieve dehydration)

Anemia and kidney disease

Decreased kidney function can lead to decreased erythropoietin production resulting in anemia

ANP (atrial) and BNP (ventricle)

Work together to lower BP

Anti-hypertensive meds

Ace inhibitors: -pril
ARBs: -sartan
Alpha blockers: -sin
Beta blockers: -olol (metoprolol)
Ca++ channel blockers: diltiazem, nifedipine, verapamil
Diuretics: furosemide, hctz, spironolactone


Increased BUN and creatinine in the blood w/o systemic s/s


Increased BUN and creatinine with multiple system organ failure

S/S of renal failure

Poor appetite
Bone pain
Stunted growth
High urine output (diuresis phase)
No urine output (oliguric phase)
recurrent UTIs
Urinary incontinence
Pallor (anemia)
Full body edema
Bleeding tendencies (d/t coagulopathy)
Poor muscle tone
Change in menta


Leading cause of kidney failure; caused by high BG levels which triggers inflammatory response.
Prominent s/s diabetes is damaging kidneys is proteinuria.

Electrolyte imbalance

Na+ loss and K+ retention in oliguric phase of renal failure

Glomerular filtration rate (GFR)

Nl range: 85-135; measure of how much blood is filtered by gomeruli every minute. Helps to detect early kidney disease (before creatinine)

(Acute) Glomerulonephritis

Inflammation of the glomerular membrane. Primary caused by untreated group A strep
2ry caused by other diseases/conditions.


Blood in urine

Kidney stones (renal calculi)

Flank pain, radiates from flank to groin, suprapubic pain
High urine concentration=stone forming. Dehydration is modifiable risk factor

Nephritic Syndrome

Inflammatory process that results in hematuria AND proteinuria

Blood urea nitrogen (BUN)

Nl range <20
Indicator of kidney damage

Nephrotic Syndrome

Permeability of glomerular pores allows large loss of protein molecules via the kidneys. Only proteinuria, no hematuria present


Decreased urine output (dehydration/kidney damage)


NO urine production (kidney failure)

Periorbital edema

When edema is severe enough the area around the eyes fill with fluid and become swollen.


Protein in urine

RAAS Response

1. Initiated by decreased perfusion to the kidneys.
2. The kidneys release renin.
3. Renin combines with angiotensinogen (from liver) to form Angiotensin I. (Occurs in blood stream)
4. Angiotensin I is converted in the lungs to angiotensin II by ACE.
5. A

Four phases of AKI

Onset: Sig blood loss, burns, fluid loss. Lasts hours to days
Oliguric: Urine output below 400mL/day. Lasts 8-14 days depending on nature of AKI
Diuretic: Occurs when AKI is corrected. Lasts 7-14 days
Recovery: Decreased edema, nl fluid/electrolyte balanc

Specific gravity

1.010-1.030; measure how dilute/concentrated urine is

Fixed specific gravity

Number never changes through multiple UAs; indicates kidneys can no long dilute/concentrate urine. Late sign of end stage kidney failure.

Renal failture (chronic)

progresses over at least 3 mo; results in permanent renal failure


Infection of lower urinary tract (bladder and urethra)

Vit D

Activated vit d allows GI tract to absorb calcium preventing hypocalcemia

6 major kidney functions

1. Filters blood
2. Maintains BP
3. Acid-base balance
4. Erythropoietin synthesis
5. Synthesis and release of renin
6. Activate vit D

What s/s would you expect to see if a person has lost protein through their urine (nephrotic syndrome)?

Edema; body will retain water when kidneys malfunction

Differences between cystitis and pyelonephritis

Cystitis: Frequency, urgency, dysuria, suprapubic tenderness
Pyelo: Fever, leukocytosis, N/V, flank pain/tenderness

What is the first s/s of kidney failure?


What are the two leading causes of CKD?

Diabetes (#1) and HTN (#2)


Brain toxic; high levels will cause change in LOC


Free fluid accumulation in the abdomen; BP can drop w/ paracentesis.

What causes ascites?

1. Portal htn
2. Damaged liver not synthesizing serum protein


Flapping tremor of the hands

Colorectal cancer risk factors

Age: 50 yrs or older
Gender: Greater in men than women
Race: Black/Caucasia
Family Hx: 25% of colon cancer
Medical Hx: Crohn's or U.C.
Diet: Unhealthy fats; refined sugars/flour, low fiber/vitamins
Other: Obesity/sedentary lifestyle/lack of exercise, smok


(Usually) caused by gallstones or biliary sludge being trapped in opening of gallbladder.


Scarring of liver tissue causing it to function abnormally.

Crohn's disease

Autoimmune disorder that can occur anywhere in the GI tract. It involves ALL layers .

Esophageal varices

Large veins in esophagus caused by obstructed blood flow from portal vein.

Gastroesophageal reflux disease (GERD)

Intense heartburn (will r/o MI when seeking tx);
Esophageal sphincter is weak and allows backflow from stomach to esophagus. (Acid damages the lining.)


Pain occurs 30-60 min after a meal
Pain worse when lying down (pts will sleep w/ head elevated)
Pain worse when bending over.

GERD risk factors

Hiatal hernia
Fatty foods

GI bleed s/s

-Bright red emesis (very dangerous, usually from esophageal varices)
-Coffee ground emesis (usually d/t partial digestion in stomach.)
Melena (black, tarry stools: equivalent of coffee ground emesis; alkaline digestive enzymes breakdown

What are some causes of a GI bleed?

Esophageal inflammation
Ulcerative colitis
Chron's disease

Hepatic encephalopathy

Damaged liver cannot break down protein; ^^ ammonia levels. Ammonia is highly brain toxic

Hepatitis A

Oral-fecal (food borne)

Hepatitis B

Blood/bodily fluid borne: Most commonly spread by unprotected sex, dirty needles, mom to baby. Major cause of liver cancer; vaccination available.

Hepatitis C

Blood/bodily fluid borne: Most commonly spread by unprotected sex, dirty needles, mom to baby.
Major cause of liver cancer. No vaccination; tx available

Hepatorenal syndrome

1. Decreased blood circulation will trigger RAAS system; causes vasoconstriction and ^BP.
2. Hepatic failure prevents removal of angiotensin; HTN will get worse if not corrected.
3. Azotemia will occur following kidney damage.
End stage renal failure.

Hiatal hernia

Protrusion of upper part of stomach through diaphragm. May be caused by a weakening of supporting tissue/structures. Usually only symptomatic if GERD is present.

Risk factors for HH

Habitual vomiting
Weight training
Smoking/alcohol use

Irritable bowl syndrome (IBS)

functional GI disorder" caused by changes in the GI tract w/ damage.


Damaged liver cannot break down bilirubin (in RBCs) depositing in the skin turning it yellow.
Stools will be white.

Liver enzymes (LFTs)

ALT/AST increase w/ damage to liver tissue

Peptic ulcer disease

Erosion of GI mucosa usually caused by H. Pylori bacteria. Occurs in 90% of duodenal ulcers.

Risk factors of PUD

Smoking (1st and 2nd)
Alcohol use


Intense itching d/t jaundice/icterus

Ulcerative colitis (UC)

Autoimmune disease that occurs in the large intestine; only involves mucosal layer

What are some complications of ulcerative colitis?

Dehydration (fluid/electrolyte imbalance)
Chronic bloody diarrhea
Unintended wt lostt
abd pain/cramping
HIGH risk for colorectal cancer

Asterixis is an early warning sign of what?

Hepatic encephalopathy

What is portal hypertension?

Increased blood pressure in the portal vein.

What is a common cause for portal htn?


What are some sx of portal htn?

Black, tarry stools
Hematemesis (emergency)
Esophageal/stomach varices

6 F's of Cholecystitis

Fair skin
Family hx

What is a warning sign of cholecystitis?

Pain immediately after eating (fatty foods).

What is the most common cause of cirrhosis?

Chronic alcohol use/abuse
*Can also be caused by hepatitis or hepatotoxic drugs (tylenol)

What are some complications of Chron's disease?

Fluid/electrolyte imbalance
Diarrhea (dehydration)


pH is NORMAL, other two values abnormal

Partially compensated

ALL values abnormal


pH and ONE other value abnormal

Hypervolemia s/s

Abd swelling
HTN/heart problems
Wt gain

hypovalemia s/s

Anxiety, pallor, confusion, oliguria/anuria, tachypnea

HypErtonics (fluid Enters blood stream)

Fluid is pulled from the tissue into the blood stream by high concentration of solutes. Large molecules (protein/glucose) attract water. Used for RAPID fluid replacement.
Ususally used in emergent situations to allow vessels to be filled to keep from losi

HypOtonics (fluid goes out of vessel)

Fluid moves from low to high concentrations . Used when tissue is dehydrated.

Isotonics (stay where I put it)

Most commonly used; fluid moves EQUALLY back and forth across a membrane w/o changing cell size.
*Preferred for fluid replacement d/t similar tonicity to blood.

Airborne precautions (You're on the air with MTV)

Precautions: private room, negative pressure when possible. 6-12 air exchanges/hour
Providers wear N95/HEPA
Pts/visitors to wear standard masks at all times
Measles (rubeola)
varicella (also use contact*)

Contact precautions (Mrs. WEE says "can't touch this.")

Precautions: Gown/gloves, shoe/hair covers as needed.
Respiratory infections
Skin infections
Enteric infections (c. diff)
Eye infections (conjunctivitis)

Droplet precautions (Mr. Pimp drops in for an unwelcome visit.)

Precautions: standard room, mask for staff and visitors. Gloves/gown/eye protection as needed.
Rubella (German measles)

Hypotonic solutions

0.45% NS
0.225% NS

Hypertonic solutions

3% saline

Isotonic solutions

0.9% NS
Lactated ringers

Calcium Ca++ (8.5-10.5)

Extracellular; CALMS muscles and nerves (Chvostek's signs)
Low Ca=laryngeal spasms
Hi Ca=muscle weakness

Sodium Na+ (135-145)

Extracellular; EXCITES nervous system
Low Na= same s/s fluid overload
Hi Na= same s/s dehydration

Potassium K+ (3.5-5.0)

Intracellular; affects cardiac tissue and GI tract
Low K=dysrhythmias, N/V, paresthesia, seizures, and constipation (calms GI)
High K=diarrhea (excites GI)

Magnesium Mg+ (1.5-3.0)

Intracellular; CALMS smooth muscle and DTRs
Low Mg= hyperreflexia
High Mg= resp failure
milk of magnesia=laxative