Pathology Unit 3, 2Nd Semester Cson

Front 1

Kidneys “filter” about how much per day?

Back 1

150 Liters

Front 2

Kidneys reabsorb what % of what they filter?

Back 2

about 99%

Front 3

How much urine does the kidneys' filtering process yield per day?

Back 3

about 1.5 Liters of urine per day

Front 4

What normally restricts bacteria from entering the bladder?
(4)

Back 4

Normal urine flow
Various antibacterial enzymes / antibodies
Normal flora in region
Mucus from glands trap bacteria

Front 5

What organism causes most uncomplicated UTIs?

Back 5

Escherichia coli (80%)

Front 6

What causes a "complicated" UTI?

Back 6

Abnormalities of urinary system or compromised immune system

Front 7

What is cystitis?

Back 7

Inflammation of bladder

an Uncomplicated UTI
(May be complicated if other disease processes are present)

Front 8

Signs/Symptoms of UTI:
(4)

Back 8

Pain on urination (dysuria)
Frequent urination
Suprapubic or lower back discomfort
Cloudy, foul smelling urine

Front 9

Signs/Symptoms of UTI in elderly:

Back 9

Confusion
Abdominal discomfort

Front 10

What is Acute Pyelonephritis?

Back 10

Infection of renal pelvis, tubules, & interstitial tissue of one or both kidneys

Front 11

2 possible causes of acute pyelonephritis:

Back 11

Causes:
Upward spread of bacteria from bladder

Spread of bacteria via bloodstream

Front 12

S/S of Acute Pyelonephritis
(6)

Back 12

Enlarged kidneys w/ abscesses
Fever / chills
Leukocytosis, bacteriuria, pyuria
Low back pain
N/V, headache, malaise
Painful urination

Front 13

What is Chronic Pyelonephritis & what does it lead to?

Back 13

Persistent, recurring infection

Leads to scarring of kidney(s)

Front 14

What increases the risk of chronic pyelonephritis?

Back 14

Kidney stones increase risk

Vesicoureteral reflux increases risk

(Exact cause is difficult to determine.)

Front 15

What causes Urinary Tract Obstruction?

Back 15

Lower urinary tract disorders
[Enlarged prostate (men), Urethral stricture, Pelvic organ prolapse (women)]

Kidney stones

Renal tumors/Bladder tumors

Front 16

What causes Urethral Stricture (Male or Female)?
(4)

Back 16

Congenital
Infection
Injury
Surgical manipulation
(Any of these may cause scarring & narrowing of lumen)

Front 17

What is Pelvic Organ Prolapse (Female)?

Back 17

Downward protrusion of bladder into vagina

Front 18

Renal Calculi (Kidney Stones)--where do they form?

Back 18

May form anywhere in urinary tract
Usually form in renal pelvis or calices

Front 19

What are kidney stones made of?

Back 19

70-80% made of calcium oxalate or calcium phosphate
(struvite, uric)

Front 20

Kidney Stones
Causes / Predisposing factors:
(7)

Back 20

Dehydration
Infection
Obstruction
Changes in urine pH
Immobilization
Diet
Metabolic factors (Ex: gout, hyperparathyroidism)

Front 21

Renal Calculi—Signs/Symptoms:
(6)

Back 21

Severe pain—may move from lower back to sides to pubic region
N/V
Often fever / chills
May have hematuria
May have abdominal distention
May have oliguria

Front 22

What Renal Tumors are the most common?

Back 22

Renal cell carcinoma (RCC) most common

Front 23

Factors associated with renal cell carcinoma:
(3)

Back 23

Tobacco use, obesity, HTN appear to be associated w/ RCC

Front 24

RCC sites of metastasis

Back 24

Usually occur in one kidney & metastasize to lungs, liver, lymph, & bone

Front 25

Where is a Renal cell adenoma (benign tumor) usually located?

Back 25

Encapsulated & located near renal cortex

Front 26

Signs/Symptoms of Renal Tumors

Back 26

Early stages are often silent

Late signs include
Hematuria
Flank pain
Palpable flank mass
Weight loss

Front 27

leading risk factor for Bladder Tumors

Back 27

Tobacco use appears to be

Front 28

Common location of bladder tumors:

Back 28

Arise from alteration of epithelial tissue at base of bladder

Often involve ureter orifices and bladder neck

Front 29

Sites of metastasis for bladder cancer:

Back 29

Usually metastasize to lymph, liver, bones, & lungs

Front 30

s/s bladder tumor:
(3)

Back 30

**Visible, painless hematuria

Pelvic or back pain may occur with metastasis

UTIs are common complications→ frequency, urgency, dysuria

Front 31

What is Glomerulonephritis?

Back 31

Inflammation of the glomerulus

Front 32

Acute glomerulonephritis is often associated w/ what disease?

Back 32

strep throat, or impetigo→develops 2-3 weeks post infection

Front 33

Chronic glomerulonephritis is often caused by what diseases?

Back 33

IDDM or Lupus erythematosus→leads to chronic renal failure

Front 34

Patho of Glomerulonephritis
(7 steps in chronic)

Back 34

Infection initiates inflammatory process→
Antigen-antibody processes deposited in glomeruli→
Nephrosclerosis develops→
(In chronic) Cortex layer shrinks→
Bands of scar tissue distort remaining cortex→
Branches of renal artery thicken→
End-stage renal disease

Front 35

s/s of Nephrotic Syndrome
(results from damages to the glomerular capillary membrane)

Back 35

**Large amounts of protein excreted in urine (proteinuria)
Decrease of albumin in blood (hypoalbuminemia)
High serum cholesterol and low – density lipoproteins (hyperlipidemia)
**Major S/S: Edema (pitting & ascites)

Front 36

Nephrosclerosis
main causes→

Back 36

Hypertension & Diabetes

Front 37

Nephrosclerosis
Decreased blood flow to kidneys→
What develops?

Back 37

Patchy necrosis develops→
Fibrosis develops; glomeruli destroyed→
Leads to End-stage renal disease

Front 38

What is Acute Renal Failure?

Back 38

Abrupt reduction in renal function w/elevation of BUN & creatinine levels

Front 39

Urine output with acute renal failure?

Back 39

Usually associated w/ urine output of
<30 ml/hr or <400 ml/day

Front 40

Is acute renal failure permanent?

Back 40

Most of the time condition is reversible

Front 41

Signs/Symptoms of ARF:
(4)

Back 41

>Oliguria begins within 1 day post hypotensive event & lasts 1 - 3 weeks
>Lethargic
>Skin / mucus membranes dry
>CNS→headache, muscle twitching, seizures
Many body systems affected
Recovery depends on how long the cause lasted

Front 42

What is ESRD?
What happens?

Back 42

ESRD is progressive, irreversible deterioration in renal function
End products of protein metabolism (normally excreted in urine) accumulate in the blood

Front 43

Causes of ESRD:

Back 43

Diabetes mellitus
HTN
Chronic glomerulonephritis
Pyelonephritis
Obstruction of urinary tract

Front 44

Signs/Symptoms of ESRD:

Back 44

>UREMIA (result of accumulation of toxins in plasma)
>HTN
>Anorexia
>Nausea / vomiting
>Diarrhea
>Weight loss

Front 45

Central Nervous System includes:

Back 45

Brain
Spinal cord

Front 46

Peripheral nervous system includes:

Back 46

Cranial nerves
Spinal nerves

Front 47

Peripheral Nervous System
Functionally → divided into:

Back 47

Somatic nervous system → pathways that regulate voluntary motor control (Ex: skeletal muscles)

Autonomic nervous system → pathways that regulate body’s internal environment via involuntary control of organ systems (Ex: heart/circulatory system)

Front 48

Autonomic Nervous System further divided into:

Back 48

Sympathetic nervous system (SNS)

Parasympathetic nervous system (PNS)

Front 49

Innervation of Organs is accomplished by:

Back 49

Autonomic Nervous System
Organs innervated by specific components of nervous system

Front 50

What are Neuroglia?

Back 50

“nerve glue” → supporting cell in CNS → provide structural support & nutrition

Front 51

What is a Schwann cell?

Back 51

supporting cell in PNS → provide structural support & nutrition

Front 52

Do mature nerve cells divide?

Back 52

Mature nerve cells do not divide

Front 53

Damaged nerve cell Regeneration in CNS limited by...

Back 53

↑ incidence of scar formation & different nature of myelin formed

Front 54

Regeneration of CNS nerve cells depends on many factors—

Back 54

location, type of injury, inflammatory response, process of scarring

Front 55

(CNS) The closer (of injury) to cell body, greater chances of

Back 55

cell dying/not regenerating

Front 56

Alterations in Arousal (state of awakeness RAS)
Caused by:

Back 56

Structural damage (trauma, vascular, infection)

Metabolic disturbances (hypoxia, electrolyte disturbances, drugs, toxins)

Psychogenic (rare--psychiatric)

Front 57

Penetrating Head/Brain Trauma has a high risk of ______________ because brain structures may be exposed to environment.

Injury to brain tissue significant

Back 57

High risk for infection

Front 58

Signs/Symptoms of Brain Trauma:
(9)

Back 58

Headache w/increasing severity
Vomiting
Drowsiness
Confusion
Seizure activity
Respiratory depression/failure
Loss of consciousness
Loss of reflexes
Pupillary dilation

Front 59

Peripheral Nerve Trauma
Signs/Symptoms:

Back 59

Numbness
Paresthesia (abnormal sensation ie. burning, pricking, tingling, tickling)
Pain

Front 60

Peripheral Nerve Trauma Cause:

Back 60

Crushing or cutting of neurons

Success for regeneration much higher in crushing injuries

Front 61

Transient ischemic attack (TIA)

Back 61

Brief period of inadequate cerebral perfusion→sudden focal loss of neurologic function
Full recovery usually within 24 hours

Front 62

Cerebrovascular accident (CVA)

Back 62

Stroke often causes permanent neurological deficits
Damage occurs within seconds to minutes due to loss of perfusion

Front 63

Signs / Symptoms of CVA:
(7)

Back 63

>Depend on brain hemisphere & location of occurrence (right brain affects left half of body)
>Loss of consciousness
>Weakness
>Difficulty speaking
>Difficulty swallowing
>Impaired vision
>Paresthesias

Front 64

Patho of Meningitis

Back 64

>Bacteria normally found in nasopharynx
>Usually starts w/upper respiratory infection → bacteria become blood borne →(thought to)enter CNS through choroid plexus → bacteria (or toxins) cause inflammation in meninges→ exudate causes thickening of CSF→ impedes flow, disrupts blood flow due to swelling

Front 65

Signs/Symptoms of Bacterial Meningitis

Back 65

>Typical symptoms for infection +
-Severe headache
-Photophobia
-Nuchal rigidity
-↓consciousness
-Seizures
-Petechial rash

>Viral symptoms usually less severe
>Fungal symptoms much slower & insidious

Front 66

Encephalitis
Cause:

Back 66

usually viral—mosquito borne viruses & herpes simplex type I

Front 67

Encephalitis Patho:

Back 67

Virus reaches meninges → edema develops → ↑ICP → widespread nerve cell degeneration

Front 68

Encephalitis S/S:

Back 68

fever, delirium, confusion → unconsciousness, seizure activity, involuntary movement, abnormal reflexes, paresis & paralysis

Front 69

Most common neurodegenerative disorder / most frequent cause of dementia in elderly

Back 69

Alzheimer’s Disease

Front 70

Alzheimer’s Disease--cause:

Back 70

Exact cause unknown → ?loss of neurotransmitter stimulation

Front 71

“Neurofibrillary tangles” & “senile plaques” found in cerebral cortex & hippocampus

Back 71

Alzheimer’s Disease

Front 72

Signs/Symptoms of Alzheimer’s Disease
(7)

Back 72

Early signs mimic natural aging processes:

Memory loss
Language loss
Confusion
Restlessness
Mood swings
Difficulty in interpreting visual information

Front 73

Parkinson’s Disease

Back 73

Chronic, progressive degeneration of neurons in the basal ganglia (corpus striatum)

Associated with impaired motor function

Onset predominantly middle to old age

Front 74

Patho of Parkinson’s Disease

Back 74

Cause: Unknown

Degeneration of nigrostriatal pathway → reduction in neurotransmitter dopamine → alters excitability of striatum & release of other neurotransmitters (acetylcholine)

Neurons in substantia nigra lose pigment & characteristic black color

Front 75

Signs/Symptoms of Parkinson’s Disease
{Most neural degeneration occurs before the onset of symptoms}

(6)

Back 75

Tremors (hands, arms, legs, face)
Rigidity
Bradykinesia (slowed movement)—may progress to akinesia (inability to move)
Postural instability
Late symptom: Dementia

Front 76

What enzyme does saliva contain & what does it help break down?

Back 76

α-amylase→CHO digestion

Front 77

Stomach:
Secrete...
(3)

Back 77

digestive juices + HCL + pepsin

Front 78

Length of Small intestine:

Back 78

5 meters long!

Front 79

3 parts of the small intestine:

Back 79

>Duodenum→Receives chyme through pyloric sphincter→bile (fats) + pancreatic enzymes (proteins, CHOs, fats) + intestinal enzymes (proteins, CHOs, fats)
>Jejunum→Sugars & proteins absorbed
>Ileum→Bile salts, Vit B12, chloride absorbed

Front 80

Parts of Large intestine: (“leftovers” enter via ileocecal valve)

Back 80

Cecum, appendix, colon (ascending, transverse, descending, sigmoid), rectum

Front 81

GI Disorders

(8)

Back 81

1) Motility disorders
2) Gastritis
3) Peptic ulcer disease
4) Malabsorption syndromes
5) Inflammatory bowel disease
6) Appendicitis
7) Vascular insufficiency
8) Disorders of nutrition

Front 82

1) GI Motility Disorders

Back 82

A) Dysphagia
B) Gastroesophageal reflux
C) Hiatal hernia
D) Pyloric obstruction
E) Intestinal obstruction

Front 83

What is Achalasia?

Back 83

nerve dysfunction→failure of muscular ring at end of esophagus to relax→lower esophagus becomes distended

Front 84

What is Gastroesophageal Reflux?

Common Symptom?

Back 84

Reflux of chyme into esophagus from stomach

Common symptom: “Heartburn”

If long term→esophageal inflammation & erosion→fibrosis & thickening

Front 85

What causes Gastroesophageal Reflux?

Back 85

Causes: Obesity, smoking, delayed gastric emptying (ulcers, pyloric stricture, hiatal hernia)

Front 86

2 types of Hiatal Hernia?
Protrusion of ↑ stomach thru diaphragm

Back 86

Sliding (congenital, short esophagus, trauma, weak diaphragm muscles)
S/S: GER, esophagitis

Paraesophageal(curvature of stomach herniates alongside of esophagus)
S/S: Discomfort after eating, dysphagia

Front 87

S/S of Pyloric Obstruction:

Back 87

S/S: (early) vague epigastric fullness—worse after meals & late in day; nausea; epigastric pain

S/S: (late) gastric distention; vomiting; infrequent, small stools

Front 88

Types of Intestinal Obstruction
(4)

Back 88

Simple: mechanical blockage
-Acute: Torsion, intussusception, herniation
-Chronic: Tumor, inflammatory disorder

Functional: ↓ motility (Ex—paralytic ileus)

Front 89

S/S of Intestinal Obstruction

Back 89

S/S: “Colicky” pain + vomiting
May become necrotic, perforate → peritonitis

Front 90

Gastritis
Inflammation of ...
Acute: Erosions usually ...
Cause:
S/S:

Back 90

gastric mucosa
superficial
Chemicals, drugs (NSAIDS)
Vague abdominal discomfort; epigastric tenderness; BLEEDING

Front 91

Cause of Chronic Gastritis:

Back 91

?Autoimmune, H. pylori

Front 92

What is Peptic Ulcer Disease?

Back 92

Break / ulceration in protective mucosal lining of stomach, duodenum

Submucosa exposed to gastric secretions → autodigestion

Front 93

What increases risk for Peptic Ulcer Disease?
(6)

Back 93

↑ Risk: Smoking, ↑ age, NSAIDS, alcohol, H. pylori, chronic diseases

Front 94

Gastric/Duodenal Ulcers
Causes:

Back 94

NSAIDS→ inhibits prostaglandins + ↓mucus production
H. pylori→ stimulates gastrin production→ ↑acid production/ulcer formation

Front 95

Gastric/Duodenal Ulcers S/S:

Back 95

Chronic intermittent pain relieved by food intake/antacid use; 1st clinical manifestation may be hemorrhage / perforation

Front 96

Malabsorption Syndromes
Interfere with nutrient absorption in small intestine
Types:

Back 96

>Pancreatic insufficiency→ Deficient production of pancreatic enzymes (affects digestion of proteins, CHO, fats)
>Lactase deficiency→ Lactose not broken down
>Bile salt deficiency→ Fats not digested / absorbed

Front 97

Inflammatory Bowel Disease
Types: (3)

Back 97

Ulcerative colitis—chronic, inflammatory→ulceration of mucosa in colon (usually in sigmoid & rectum)

Crohn disease—inflammatory, affects both small & large intestine (rectum is seldom involved)

Diverticular disease—herniations / saclike outpouchings of mucosa thru muscle layers (usually wall of sigmoid colon)

Front 98

Appendicitis

Back 98

Inflammation of vermiform appendix
Most common surgical emergency of abdomen
Generally 20-30 years of age (can happen at any age)

Front 99

Appendicitis--Cause:

Back 99

?obstruction of lumen w/stool, foreign bodies, tumors → bacterial infection
Obstruction → appendix can’t drain → ↑pressure → appendix becomes hypoxic → mucosa ulcerates → bacteria invasion → inflammation → gangrene → perforation

Front 100

What are the 3 main accessory organs that aid digestion?

Back 100

Liver, GB, Pancreas

Front 101

Liver Structure

What encapsulates the liver (blood vessels, lymphatics, nerves)?

Back 101

Glisson capsule

Front 102

What carries oxygenated blood to the liver?

Back 102

Hepatic artery

Front 103

What does the hepatic portal vein deliver to the liver?

Back 103

some oxygen + nutrients

Front 104

Functional cells of liver:

Back 104

Hepatocytes

Front 105

Capillaries between plates of hepatocytes:

Back 105

Sinusoids

Front 106

Kupffer cells:

Back 106

mononuclear phagocyte system

Front 107

Disse space:

Back 107

hepatic lymph system

Front 108

What channels conduct bile to bile ducts?

Back 108

Bile canaliculi

Front 109

Common bile duct empties into:

Back 109

Sphincter of Oddi

Front 110

Liver Function #1

_____________ blood

Back 110

Filters/detoxifies

Front 111

Liver Function #2

Removes _________ from body fluids
Process called _________ (amino acids converted to carbohydrates, or ketoacids, by removal of ammonia)
Converts to ______, then passes into the blood
Excreted in ________

Back 111

ammonia
deamination
urea
urine

Front 112

Liver Function #3

Produces ______

Emulsifies fats

Helps in absorption of fats

Back 112

bile

Front 113

Liver Function #4

Produces plasma ________
Albumins and globulins
Maintains blood volume & pressure

Synthesizes nonessential ___________
AST, ALT, LDH, alkaline phosphatase

Can store _________ for several years

Back 113

proteins
amino acids
vitamin A

Front 114

Liver Function #5

Plays important role in ___________ metabolism
Releases _________ during hypoglycemia
Takes up _________ during hyperglycemia

Back 114

carbohydrate
glucose
glucose

Front 115

Liver Function #6

Converts glucose to glycogen: ______________
Stores it for fuel for muscles
Or, converts glucose to fat
Can convert amino acids & glycerol to glucose: ___________

Back 115

Glyconeogenesis
Gluconeogenesis

Front 116

Liver Function #7

Stores essential _______
Iron (as______) & copper
Vitamin B12 & __—stores for several months
Vitamins __ & K

Back 116

nutrients
ferritin
D
E

Front 117

Liver Function #8

Stores _______
Used to produce ATP (for cellular use)

Converts excess sugars to ______
Stored in _________ tissue

Back 117

fats
fats
adipose

Front 118

Liver Functions #9, #10, #11

Storage of large volumes of _______
Removal of ________ & foreign particles
Synthesizes prothrombin, fibrinogen, ________ I, II, VII, IX, X

Back 118

blood
bacteria
factors

Front 119

Liver Function #12

Metabolism of _________
-By-product of destruction of old rbc’s
-Gives ______ greenish black color
-Produces yellow tinge of _________

Back 119

bilirubin
bile
jaundice

Front 120

Damage tends to be most severe in Hepatitis ___ & Hepatitis ___
Hep B can result in acute _________ hepatitis

Back 120

B; C
fulminating

Front 121

3 Phases of Viral Hepatitis:

Back 121

Prodromal phase

Clinical (Icteric) phase

Recovery phase

Front 122

Prodromal phase—begins about _______ post exposure; ends w/appearance of _________

Back 122

2 weeks
jaundice

Front 123

Clinical (Icteric) phase—begins________ after prodromal phase; lasts _________

Back 123

1-2 weeks
2-6 weeks

Front 124

Recovery phase—begins w/ resolution of jaundice, about ____________ post exposure

Back 124

6-8 weeks

Front 125

Fulminant hepatitis results in...

May occur as complication of:
HCV infection
HBV infection
Combination HBV / HDV infection

Rarely occurs with HAV infections

May also occur as a result of:
Toxic reactions to drugs (eg. Tylenol)
Congenital metabolic disorders

Back 125

severe liver impairment / necrosis of liver cells
High potential for liver failure

Front 126

Fulminant hepatitis may occur as complication of:

Back 126

HCV infection
HBV infection
Combination HBV / HDV infection

Rarely occurs with HAV infections

May also occur as a result of:
Toxic reactions to drugs (eg. Tylenol)
Congenital metabolic disorders

Front 127

Hepatic necrosis is _____________

Back 127

irreversible, 60% to 90% die (fulminant hepatitis)

Front 128

Chronic liver disease—develops slowly
Widespread destruction of hepatic cells + collapse of supporting structure
Replaced by fibrous cells
Liver develops “cobbly” appearance

Back 128

cirrhosis

Front 129

Most common form of cirrhosis:

Back 129

Most common:
Laennec’s (also called alcoholic, portal, fatty cirrhosis)

Front 130

Alcoholic (Laennec’s) cirrhosis
PATHO:

Back 130

Alcohol transformed into acetaldehyde

Excessive acetaldehyde:
↓hepatocyte function
↓oxidation of fatty acids
↓enzyme/protein synthesis
↓ammonia breakdown
↓proteins leaving liver (albumin…)
↓metabolism of vitamins/minerals (malnutrition)

Front 131

With Laennec's cirrhosis, if alcohol consumption is stopped...

Back 131

Fatty accumulation in liver is reversible

Front 132

Alcoholic cirrhosis—symptoms

Back 132

>Enlarged liver (initially—fatty infiltration
>Many of same s/s of hepatitis (fatigue, anorexia, nausea, etc)
>Later s/s—ascites, esophageal varices, testicular atrophy, splenomegaly

Front 133

Postnecrotic cirrhosis

Develops from _______ hepatitis
Exposure to arsenic, carbon tetrachloride, other _________
More common in _______
Most _________ type worldwide

Back 133

chronic
toxins
women
common

Front 134

S/S of primary biliary cirrhosis:
(no known cause)

Back 134

Pruritis/hyperbilirubinemia/jaundice→light-colored stools → cirrhosis → portal hypertension→encephalopathy

Front 135

Secondary biliary cirrhosis is due to...

Back 135

Prolonged obstruction of bile duct branches / common bile duct (obstruction of stricture)

Front 136

Which metabolic diseases can cause cirrhosis?

Back 136

Wilson’s disease

Alpha¹-antitrypsin

Hemochromatosis