Last Test GI, Neuro, Skin Flashcards

Question 1

Q

What is the function of cholecystokinin?

Answer

A

Secreted from I cells in Jejunum in response to fat substances, stimulates gallbladder to release bile (breaks down fat) and pancreas to secrete digestive enzymes. Stimulates gallbladder and pancreas

Question 2

Q

Which cells in the stomach produce intrinsic factor necessary for B12 absorption?

Answer

A

Parietal Cells

Question 3

Q

All of the following statements are correct regarding pancreatic secretions EXCEPT: Amylase digests polysaccharides Trypsin digests proteins Lipase digests lipids Bile digests carbohydrates

Answer

A

Bile does not digest carbohydrates, Bile digests fats

Question 4

Q

What is the main function of the large intestine

Answer

A

Water and electrolytes are primarily absorbed

Question 5

Q

Normal hepatic function does not include:

Answer

A

Production of bile for carbohydrate digestion

Question 6

Q

PNS (peripheral) control in the GI tract increases or decreases GI motility and secretions?

Answer

A

Increases motility/secretions

Question 7

Q

Cleft Lip and Palate Risk Factors - Cause When can it be detected on a U/S

Answer

A

Genetic, maternal medications, alcohol, smoking, vitamin deficiencies Can be detected on U/S at 12 weeks

Question 8

Q

Cleft Lip vs Cleft Palate Clinical Manifestations

Answer

A

Lip: Opening in maxillary process & upper lip (doesn’t fuse) Palate: Failure of hard & soft palate to fuse

Question 9

Q

Esophageal Atresia Diagnosis

Answer

A

Cannot detect congenital on U/S although a clue would be polyhydramnios X-ray to diagnose

Question 10

Q

Esophageal Atresia Clinical Manifestations

Answer

A

Will be detected immediately after birth - drooling, vomiting, scaphoid abdomen, distended abdomen with TEF due to air

Question 11

Q

Esophageal Atresia Patho

Answer

A

Congenital malformation of the esophagus Two separate esophageal sections not connected Associated with tracheoesophageal fistula

Question 12

Q

Pyloric Stenosis Patho

Answer

A

Narrowing and obstruction of the pyloric sphincter (stiff muscle fibers) Risk factors: Macrolides in pregnancy (Zithromax/Biaxin). Olive sized mass in babies

Question 13

Q

Pyloric Stenosis Clinical Manifestations

Answer

A

Noted at birth Hard olive-shaped mass in abdomen palpated. Projectile vomiting after meals, very hungry. Failure to gain weight, dehydration In adults causes, delayed gastric emptying can cause vomiting

Question 14

Q

Dysphasia Mechanical Obstruction

Answer

A

Mechanical – esophageal stenosis; esophageal diverticula, esophagitis, tumor Extrinsic - tumor, goiter, mass Intrinsic - inside the esophagus

Question 15

Q

Dysphasia Neurological Disorders

Answer

A

Neurological – CVA, Parkinson, Alzheimer, MS, ALS, Muscular, Muscular dystrophy Any disease that changes muscle fx

Question 16

Q

Dysphasia Functional

Answer

A

Functional – Sensation with no structural cause Feels like “I can’t swallow” without any cause

Question 17

Q

Dysphasia Iatrogenic

Answer

A

Iatrogenic – Radiation, muscle relaxants, sedatives, NSAIDs, neck surgery

Question 18

Q

Vomiting Pathology

Answer

A

Vomiting Reverse peristalsis with obstruction Stimulation of infection or chemicals ICP, Pain, Migraines Should have nausea first Gastric, Duodual Ulcer, Varicies – Blood Obstruction – Bile Undigested food – Pyloric stenosis, Obstruction, Gastroparesis

Question 19

Q

Hiatal Hernia Pathogenesis & Risk Factors & Clinical Manifestations

Answer

A

Defect in diaphragm allowing a portion of the stomach to come up above diaphragm into the thorax. Risks: older age, smoking, obesity, increased abdomen pressure (heavy lifting, straining) Clinical Manifestations: Reflux inflammation of esophagus - heartburn, belching, chest pain, dysphagia. Worse sx with positioning, fullness after eating, epigastric pain

Question 20

Q

GERD Pathogenesis Risk factors & Clinical Manifestations

Answer

A

Pathophysiology -Abnormal Lower Esophageal Sphincter relaxation, Gastroparesis Risk Factor Obesity, smoking, alcohol, caffeine; hiatal hernia Medications – beta blockers, sedatives, calcium channel blockers, anticholinergics Clinical manifestations Heartburn, regurgitation of food, nausea Dry cough, laryngitis, pharyngitis Lump sensation in the throat; dysphagia Diag with Bravo pH test

Question 21

Q

Barrett Esophagus

Answer

A

Cells adapt to inflammation by becoming another type of cell Normal healthy tissue is replaced by COLUMNAR TISSUE. HIgh risk of CA - esophageal strictures

Question 22

Q

Two types of abdominal pain

Answer

A

Visceral Pain: diffuse poorly localized, gnawing, burning r/t inflammation Somatic Pain: Sharp, pinpoint pain

Question 23

Q

Esophagitis Clinical Manifestations

Answer

A

Difficult swallowing Painful swallowing Chest pain, particularly behind the breastbone, that occurs with eating Swallowed food becoming stuck in the esophagus (food impaction) Heartburn Acid regurgitation

Question 24

Q

Gastric Reflux Clinical Manifestations

Answer

A

A burning sensation in your chest (heartburn), usually after eating, which might be worse at night. Chest pain. Difficulty swallowing. Regurgitation of food or sour liquid. Sensation of a lump in your throat. Burping

Question 25

Q

Acute Gastritis Patho and Clinical Manifestations

Answer

A

Inflammation of the stomach’s mucosal lining with neutrophil infiltration Pathophysiology Infections - bacterial (H. pylori, E Coli) or viral Ingestion of irritating substances Alcohol, Aspirin, NSAIDs Excess HCL acid secretion Bile reflux into the stomach Manifestations Nausea Epigastric pain

Question 26

Q

Chronic Gastritis Patho and Clinical Manifestations

Answer

A

Pathophysiology Presence of lymphocytes, plasma cells, and macrophages Progresses from superficial inflammation to deeper mucosal gland dysfunction Gastric atrophy – glandular loss (shrinks) Clinical Manifestations: Dull , epigastric pain, nausea, sensation of fullness, anorexia, hematemesis

Question 27

Q

Type A Chronic Gastritis

Answer

A

Gastritis affecting the fundus and body Autoimmune, destroys parietal cells (HCL acid, intrinsic factor. This can cause a B12 deficiency

Question 28

Q

Type B Chronic Gastritis

Answer

A

Gastritis affecting the Antrum of the stomach. H-pylori embeds in the mucosal layer Alcohol smoking and NSAID use

Question 29

Q

What is the best way to test for H-pylori

Answer

A

Breath and Stool Blood tests are IgG and test only for past infection

Question 30

Q

Gastric and Duodenal Ulcers Patho Clinical Manifestations

Answer

A

Stomach and duodenal lesions extending through muscularis mucosae due to imbalance of destruction and protection Epigastric or RUQ pain, nausea GI hemmorhage, perforation

Question 31

Q

Gastric Ulcers

Answer

A

Gastric >50 yo, Increases with age; increased NSAID use ***Pain on empty stomach that worsens with eating Epigastric pain

Question 32

Q

Duodenal Ulcer

Answer

A

Duodenal Younger age, excess acid, H. Pylori ***Pain relieved by eating and occurs 2-3 hours later RUQ pain

Question 33

Q

Zollinger-Ellison Syndrome

Answer

A

Younger 20-50 years old Excessive gastrin secretion – gastric acid Diarrhea due to excess acid

Question 34

Q

Gastroparesis Pathology

Answer

A

Paralysis of the stomach Parasympathetic nervous system stimulates the vagus nerve PNS dysfunction causes decreased motility of the stomach

Question 35

Q

Gastroparesis Clinical Manifestations

Answer

A

Vomiting due to Delayed emptying Nausea Fullness Causesd by diabetic neuropathy and narcotics

Question 36

Q

Biliary Tree

Cystic duct from gallbladder communicates with hepatic duct to make the common bile duct which empties into the duodenum

Answer

A

Cystic duct (only affects the gallbladder) from gallbladder communicates with hepatic duct to make the common bile duct which empties into the duodenum Sphincter of Oddi is low and probably will affect the gallbladder and the liver

Question 37

Q

Cholelithiasis Pathogenesis

Answer

A

Pathogenesis: Supersaturation of bile with hypomobility and cholesterol causing precipitation of cholesterol Hypomotility (stasis of bile) allowing stone growth

Question 38

Q

Risk factors for Cholelithiasis

Answer

A

Risk factors: Fair-skinned, women Obesity, rapid weight loss Oral contraceptives

Question 39

Q

Cholelithiasis Clinical Manifestations

Answer

A

Clinical manifestations Small stones - asymptomatic Large/multiple stones – Biliary Colic Sharp RUQ/epigastric pain radiating to right shoulder Precipitated by a meal Nausea, vomiting Diaphoresis

Question 40

Q

Diagnostic Tests for Cholelithiasis

Answer

A

HIDA Scan – GB function ERCP – invasive, scope passed into duct MRCP – noninvasive MRI

Question 41

Q

Acute Cholelithiasis Clinical manifestations

Answer

A

Acute cholecystitis Gallbladder inflammation from obstruction Severe, steady pain > 4 hours Nausea and vomiting Fever, Leukocytosis Positive Murphy’s sign

Question 42

Q

Acute Cholangitis

Answer

A

Acute cholangitis Gallstones in the common bile duct Charcot Triad – fever, pain, jaundice Elevated liver tests Can progress to acute pancreatitis

Question 43

Q

Murphy’s Sign

Answer

A

Used to diagnose cholelithiasis While palpating the liver have take in and hold a deep breath. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.

Question 44

Q

Hepatitis Pathogenesis

Answer

A

Pathogenesis - Inflammation of the liver Infections – usually viral Alcohol Medications Autoimmune disease – SLE, Scleroderma May be acute, chronic, or fulminant

Question 45

Q

Jaundice Pathogenesis

Answer

A

Green-yellow staining of tissues by bilirubin Pathogenesis: Impaired bilirubin metabolism Damaged RBCs release hemoglobin Heme and globin separate into free unconjugated bilirubin Liver conjugates into water soluble bilirubin which is released into plasma In correct process, we go from unconjugated to conjugated bilirubin

Question 46

Q

Pre Hepatic Causes - Jaundice

Answer

A

Hemolysis, ineffective erythropoiesis, resorption of large hematomas

Question 47

Q

Hepatic causes - Jaundice

Answer

A

Dysfunction of liver cells: increased levels of unconjugated bilirubin

Question 48

Q

Post Hepatic causes - Jaundice

Answer

A

Mechanical obstruction in bile duct causes conjugated hyperbilirubinemia

Question 49

Q

Gilbert Syndrome Pathogenesis

Answer

A

Benign Syndrome High Bilirubin Normal Bilirubin 0.1-1 patients with this have Bilirubin 2-3 range Genetic and no associated jaundice

Question 50

Q

Hepatitis A (HAV) Pathology

Answer

A

RNA virus spread by fecal-oral route (enteric) 2- to 7-week incubation period Clinical Manifestations (last 2 weeks) Abrupt onset Jaundice (not everyone gets it), RUQ pain, malaise, anorexia, nausea, low-grade fever, children may not experience jaundice Followed by jaundice lasting approximately 2 weeks Self-limited course

Question 51

Q

Hepatitis A (HAV) Testing and Prevention

Answer

A

Serologic testing Anti-HAV IgM (acute infection) Anti-HAV IgG (previous infection) Prevention Careful handwashing Segregation Cleaning of laundry and personal items Immunization – 2 doses 6-12 months apart ***Exposure – passive human immunoglobulin within 2 weeks of being exposed***

Question 52

Q

Hepatitis B (HBV) Patho and Risk Factors

Answer

A

Partially double-stranded DNA virus Parenteral contact with infected blood or blood products, sexual contact Risk Factor Health care settings (3%); transfusions and dialysis (1%); acupuncture, tattooing, residence in an institution

Question 53

Q

Hepatitis B (HBV) Course of disease with clinical manifestations

Answer

A

Incubation period of 2-5 months (avg 90 days) Prodromal period Asymptomatic or rashes, arthralgia, arthritis, angioedema, serum sickness, glomerulonephritis, jaundice Positive for Hepatitis B DNA for more than 6 months classified as chronically infected

Question 54

Q

Hepatitis (HBV) Serologic Testing Surface antigen (HBsAg)

Answer

A

Surface antigen (HBsAg): first to appear; 1-9 weeks; actively contagious. Becomes negative once recovered HBsAg (antigen) resolves and not detected after 6 months May be transiently + 1-2 weeks after vaccine

Question 55

Q

Hepatitis (HBV) Serologic Testing Surface antibody (HbsAb - anti HBs)

Answer

A

Surface antibody (HbsAb – anti-HBs), becomes + after HBsAg disappears. Indicates recovery with immunity *** (+ after 3 doses of vaccine)***

Question 56

Q

Hepatitis (HBV) Serologic Testing Core Antibody (HBcAb - anti-HBc)

Answer

A

Core antibody (HBcAb – anti-HBc): seroconversion at 3-5 weeks and ****remains positive indefinitely implying past infection***

Question 57

Q

Hepatitis (HBV) Serologic Testing Hepatitis B e antigen (HBeAg)

Answer

A

Hepatitis B e antigen (HBeAg): active viral replication and ***highly infective ***

Question 58

Q

Hepatitis (HBV) Serologic Testing Hepatitis B e antibody (HBeAb) anti Hbe

Answer

A

Hepatitis B e antibody (HBeAb) – minimal replication and decreased infectivity - chronic

Question 59

Q

Hepatitis B Titers

•Acute:

HBsAg – (surface antigen) – appears first

HBcAb IgM (core Ab) – seroconverts early

HBsAb – (surface Ab) recovered and/or

has immunity from vaccine (anti-HBs)

HBeAg - very infective

HBeAb - minimally infective

Total anti-HBc – positive indefinitely

•Chronic:

HBsAg - remains positive 6 months after infection

HBsAb (anti-HBs) NEGATIVE - never becomes positive

Total anti-HBc – positive indefinitely (IgG)

Hepatitis B DNA remains positive

Answer

A

HBsAg (antigen) resolves and not detected after 6 months Surface AB (anti-HBs) detected - recovered long term Total Anti HBc - always present if there once was an infection HBeAg - contagious initially anti-Hbe - means less or not contagious due to resolving

Question 60

Q

Hep B

Answer

A

Small window period where only the Total and IgM anti-HBc is detected as the disease moves from acutely infected into the resolved phase In the resolved phase, the IgM anti-HBc will go away and the anti-HBs (AB) will appear

Question 61

Q

Acute Hepatitis B Titers

Answer

A

Acute: HBsAg – (surface antigen) – appears first HBcAb IgM (core Ab) – seroconverts early HBsAb – (surface Ab) recovered and/or has immunity from vaccine (anti-HBs) HBeAg - very infective HBeAb - minimally infective Total anti-HBc – positive indefinitely

Question 62

Q

Hepatitis Titers Chronic

Answer

A

Chronic: HBsAg - remains positive 6 months after infection HBsAb (anti-HBs) NEGATIVE - never becomes positive Total anti-HBc – positive indefinitely (IgG) Hepatitis B DNA remains positive

Question 63

Q

Hepatitis B Diagnostic Testing

Answer

A

+ test for HBeAG or HBsAg or HBV DNA on 2 samples 6 months apart –or– test for HBeAg, HBsAg, HBV DNA and - for IgM anti HBC

Question 64

Q

Hepatitis C (HCV) Pathology

Answer

A

Single-stranded RNA virus Spread blood contact High risk - IV drug use or blood transfusions prior to 1990 Insidious onset usually Have 6 types Type 1: most common in the United States but has a lower response rate to treatment Types 2 and 3: common in N. America Types 4 to 6: common overseas

Answer 65

A

Acute HCV infection Usually asymptomatic – mild viral symptoms Brief elevated liver enzymes Chronic HCV infection Usually asymptomatic until advanced liver disease intervenes Permanent liver enzyme elevation ***Most common cause of end-stage liver disease with cirrhosis*** ***Test Anti-HCV to detect HCV RNA by PCR to measure levels of viral load

Answer 66

A

Hepatitis D is a incomplete virus that requires the helper function of HBV to replicate Hepatitis E is not found in the US high mortality for pregnant women

Answer 67

A

Asymptomatic incubation phase (infectious) Prodromal phase 2 weeks after exposure Low grade fever, fatigue (feels like flu), headache Nausea, vomiting, abdominal pain Icteric phase Jaundice Pruritus Clay colored stools, dark urine (bilirubin goes into urine not stool) Hepatomegaly Recovery phase 6-8 weeks after exposure

Answer 68

A

Inflammation of the liver parenchyma Caused by many viruses Cytomegalovirus, Epstein–Barr “Viral hepatitis” Hepatitis A - “infectious hepatitis” Hepatitis B - “serum hepatitis” Hepatitis C Hepatitis D (Delta) – defective RNA virus Hepatitis E

Answer 69

A

Pathogenesis Active inflammation of the centrilobular region of the liver Liver cells show pathologic changes of hepatocyte necrosis with neutrophilic infiltration (Mallory bodies). Causes Alcoholics binge in larger quantities than usual.

Answer 70

A

Diagnosis AST (SGOT) markedly > ALT (SGPT) Mortality rate 33%

Answer 71

A

Damage to the liver resulting in decreased liver function Chronic, progressive, irreversible, diffuse Results in fibrosis, nodular scarring Most frequent causes Hepatitis C infection and chronic alcohol abuse Hepatic venous obstruction due to RHF Hemochromatosis NAFLD due to rising obesity

Answer 72

A

Highly linked to obesity Spectrum of liver diseases which originate from nonalcoholic fatty liver disease (NAFLD) and progresses to fibrosis and cirrhosis. Liver has excessive buildup of triglycerides in the hepatocytes without consumption of alcohol or idiopathic liver disease and viral infection Fat deposition in the liver along with inflammation which can progress to liver failure

Answer 73

A

Manifestations Early disease is asymptomatic Intermittent upper quadrant pain, weakness, fatigue, anorexia Diag: U/S shows echogenicity (fatty)

Answer 74

A

Clinical manifestations

•Ammonia level correlates positively with the level of encephalopathy
•Dementia
•Psychotic symptoms
•Spastic myelopathy
•Asterixis “liver flap” (classic sign)
•Spastic jerking of hands held in forced extension
•Mild confusion and lethargy to stupor and coma (Grade 1 to 4)

Answer 75

A

Autosomal recessive disorder prominent in Europeans

Activity of mutant gene (HFE) this allows excessive and uncontrolled iron absorption.

Fe deposits in the liver, pancreas, and heart, can lead to liver failure

High level of iron in plasma and serum

Answer 76

A

0 - AOx3, NO Asterixis

1 - mild confusion. Can detect Asterixis

2 - Lethargy with inappropriate behavior. Obvious Asterixis

3 - Somnolent with incomprehensible speech and marked confusion

4 - COMA

Answer 77

A

Congested venous drainage of the GI tract
Clinical manifestations
Anorexia
Varices (esophageal, gastric, hemorrhoidal) can rupture; cause uncontrolled bleeding

Ascites

Answer 78

A

Variceal bleeding
30% will have hemorrhage within 2 years
Mortality 50%

The greatest risk of rebleed occurs in first 72 hours

Answer 79

A

Causes:

Cholelithiasis - #1 cause
Alcohol abuse
Biliary dysfunction
Hypertriglyceridemia = >600
Pancreatic tumor

Answer 80

A

Manifestations

Steady, boring pain in epigastric area or LUQ worse after eating
- Increases in intensity
- Severe tenderness on palpation
- Radiates or penetrates to back
- Nausea and vomiting
Abdominal distention
- Hypoactive bowel sounds
- Low-grade fever

Medical emergency with 15% mortality due to pseudocyst/abscess rupture and peritonitis

Answer 81

A

Labs

Amylase – rises within 12 hours; lasts 5 days
Lipase – rises within 8 hours; lasts 14 days
C reactive protein – (CRP) immune
CMP – LFT changes, bilirubin
CBC - infectious
Triglyceride level
CT or MRI ABD

Answer 82

A

Higher incidence in alcohol abuse

Pathogenesis

Presence of chronic inflammatory lesions in the pancreas
Key element: necrosis of exocrine parenchyma followed by fibrosis
Leads to calcification—obstructed flow of pancreatic juices
Persistence of symptoms secondary to pancreatic dysfunction over weeks and months

Answer 83

A

Clinical manifestations

Bouts of acute pancreatitis with progressive endocrine and exocrine pancreatic dysfunction
Diabetes: progressive loss of pancreatic islets
Malabsorption: fat and vitamins A, D, E, and K
Weight loss: poor intake related to pain
Insidious onset of steady, boring epigastric pain radiating to back (first symptom)
Nausea

After about 5 years of continual pain: decrease in symptoms (pain “burns out”)

CT best for diagnosis

Answer 84

A

Small Intestine - 5-6 meters long

Absorbs most of the nutrients

Duodenum, Jejunum, Ileum

Ileocecal valve – separate ileum from colon

COLON – 1.5 meters long

Ascending , Transverse, Descending

Sigmoid to rectum

Answer 85

A

Acute - < 14 days

Chronic - > 4 weeks

Acute onset

Infectious cause – viral, bacterial, parasitic
Giardia, Salmonella, C Diff, Shigella
Medications
Anxiety

Chronic occurrence

Crohn disease
Ulcerative colitis
Celiac disease

Answer 86

A

ABD pain -RLQ pain with small intestine

Small intestine – large, watery, provoked by eating

Melena black tarry stools - upper GI, small bowel or right colon

Answer 87

A

Clinical Manifestations

ABD pain - LLQ pain with large intestine
Large intestine – small and frequent, more often bloody and mucous with stool
Hematochezia - Bright red blood from lower colon (diverticulitis, hemmhoroids)
Colonoscopy can only show large intestine; cannot pass ileocecal valve

Answer 88

A

decreased fluid intake or excessing absorption

slow motility

medications

decreased fiber diet

spinal cord injury

Answer 89

A

Manifestations

Intensifying pain near the umbilicus initially then localization to RLQ (McBurney Point), worse with movement
Anorexia
Nausea
Vomiting
Fever, chills, leukocytosis

Answer 90

A

Inflammation of the vermiform appendix
Occurs as a result of obstruction

Answer 91

A

Inflammation of the peritoneum

Pathogenesis

Chemical irritation – rupture GB or spleen
Direct organism invasion – appendicitis, abscess

Answer 92

A

Classic manifestation

Abdominal rigidity
Rebound tenderness
Nausea and vomiting
Fever, Leukocytosis

Answer 93

A

Pathogenesis

Inflammation and atrophy of the intestinal villi reduces surface area
Defect in intestinal enzyme needed to digest gliadin
Decreased brush border enzymes
Impaired nutrient absorption

Answer 94

A

Inherited, autoimmune, malabsorption disorder - intolerance of gluten-containing foods
More common in females and Caucasians; children

Answer 95

A

Clinical Manifestations

Abdominal pain, bloating, gas
Diarrhea, odor
Steatorrhea
Weight loss
Vitamin Deficiencies – fatigue, hair loss

Answer 96

A

Intestinal Biopsy

Anti-tissue transglutaminase antibody - anti-ttG - tTG-IgA

Gliadin Antibodies - IgA and IgG

Stool fat absorption test

Persistent Celiac dysfunction increases risk for intestinal malignancy

Answer 97

A

Dumping of stomach contents into small intestine because of impaired gastric emptying - common after gastrectomy and gastric surgery
Loss of pyloric sphincter regulation
Common after gastrectomy and gastric surgery for the control of obesity, ulcers or cancer
Large volume of food dumped rapidly into the small intestine without chemical breakdown from the stomach
Diarrhea and abdominal pain
Rebound hypoglycemia - because body releases 2nd phase insulin release but so rapid glucose doesn’t get absorbed

Answer 98

A

Short-Bowel Syndrome

Develops after surgical removal of large portions of small intestine
Rapid transit time and reduced surface area for absorption (if ileocecal valve removed)
Diminished ability to absorb nutrients
Severe diarrhea and significant malabsorption; electrolyte imbalances

Removal of large intestine = DIARRHEA

Removal of small intestine = MALABSORPTION

Answer 99

A

Chronic inflammation of the GI tract

Crohn’s Disease
Ulcerative Colitis
Discovered at young age
Abnormal immune response to intestinal microbiota
- Alterations in epithelial barrier and immune cells
- Abnormal secretion of immune related mediators

Answer 100

A

Onset adolescent to young adult

Pathogenesis

Slow progressive T cell Inflammation through all the layers of the intestinal wall; lymphatic structures become blocked with development of deep linear ulcers; area then becomes fibrotic - cobblestoning
Deep fissures may develop into fistulas
Lumen becomes narrowed, potentially obstructed
Affects ileum, terminal ileum (most common), and proximal colon. Can affect multiple areas along the entire GI tract with normal areas in between the diseased portions.

Answer 101

A

Ascending Colon

Answer 102

A

Last section of the small bowel

Answer 103

A

Clinical Manifestations:

Constant abdominal pain in the RLQ
Occasionally there is a palpable mass in the RLQ
Hematochezia (less than UC)
Diarrhea
Weight loss

Complications

Vitamin deficiencies, anemia, malnutrition
Electrolyte imbalances
Fistulas, bowel obstructions,

Answer 104

A

Pathogenesis

Begins as T cell inflammation of the colon lining resulting in damage and necrosis; abscess formation in crypts; abscesses develop into large ulcerations develop in epithelium
Colon lining bleeds due to damage
Exacerbations and remissions

Answer 105

A

Clinical Manifestations:

Hematochezia
- Melena
Loose stools/diarrhea
Abdominal cramping
Fluid and electrolyte imbalances
Anemia
Weight loss

Answer 106

A

Pathogenesis

Bowel pattern alterations and abdominal pain with no structural or biochemical abnormalities
Increased intestinal motility and contractions

Answer 107

A

Clinical manifestations

Abdominal distension, fullness, flatus, and bloating relieved with defecation
Mucous in stool - nonbloody
Chronic and frequent constipation/diarrhea
Food intolerance may be present

Answer 108

A

Based on clinical presentation and exclusion of other GI disorders
Colonoscopy
IBS –D - irritable bowel with diarrhea
IBS – C - irritable bowel with constipation

Answer 109

A

Diverticulosis - Presence of diverticula (herniations) in the colon

More common in the descending & sigmoid colon (left side) can be right

Increases >60 yo

Low fiber, high fat diet increases risk

Asymptomatic

Diverticulitis - Pocketed food in diverticula cause inflammation and necrosis - acute infection

LLQ pain, fever, abd. distension, occasional blood in stool

Answer 110

A

Acute Diverticulitis - no colonoscopy

Bowel perforation

Peritonitis

Answer 111

A

Zankurs

Asymptomatic unless large
Gurgling in the throat, dysphagia
Risk for aspiration

Answer 112

A

Meckles

Mostly asymptomatic
Risk for ulceration and bleeding due to retained acid in the diverticulum

Answer 113

A

Squamous cell carcinomas of tongue and mouth floor

Influence of tobacco and alcohol (75%)

Men more than women

Pathogenesis

HPV lesions
Leukoplakia or erythroplakia (premalignant lesions)
Progress to nodular or ulcerative lesions

Answer 114

A

Squamous or Adenocarcinoma

Men more than women (3x)

Risk factors

Genetic, chronic severe reflux, smoking, alcohol

Pathogenesis

Chronic irritation of the distal esophagus leads to cellular dysplasia
Barrette esophagus to adenocarcinoma
EGD if GERD >5 years

Answer 115

A

Adenocarcinoma

Risk

Preserved and smoked foods
H. Pylori untreated
Smoking and alcohol
Genetics

Pathogenesis

Localized tissue inflammation advances to dysplastic cells

Answer 116

A

Commonly a secondary tumor that has metastasized (breast, lung, GI)
Can be a primary site - hepatocellular

Pathogenesis

Chronic cirrhosis, HBV, or HCV lead to hepatocellular carcinoma (primary)

Answer 117

A

Pathogenesis

Aggressive malignancy,
ductal adenocarcinoma arising from exocrine cell
Can quickly spread to nearby structures

Clinical Manifestations - usually delayed

Upper abdominal pain
Indigestion, nausea
Early satiety, anorexia
Jaundice, steatorrhea, clay colored stools

Answer 118

A

Cellular type

Hyperplastic - benign (will never become malignant)
Adenomatous - malignant potential (initially benign but if not removed can become malignant and advance to adenocarcinoma)

Answer 119

A

Sessile polyp: raised protuberance with a broad base, harder to remove. A sessile polyp that is adenomatous type is even a bigger concern
Pedunculated polyp: attached to bowel wall by a stalk that is narrower than the body of the polyp

Answer 120

A

Colon cancer screening guidelines; for the individual at average risk, colonoscopy every 10 years starting at age 45- new guideline starts age 45
Family history colon cancer - Start colonoscopy 5 years earlier than age at diagnosis
Important hereditary condition
Familial adenomatous polyposis (FAP)
At least three close relatives with colorectal cancer, colorectal cancer involving at least two generations, and one or more cases of colorectal cancer occurring before age 50 years

Answer 121

A

Risk factors

Increases after age 40
High-fat, low-fiber diet
Polyps
Chronic irritation or inflammation
Hereditary

Answer 122

A

Clinical manifestations

Change in bowel habits or new onset constipation
Right side: black, tarry stools
Left side: intermittent abdominal cramping and fullness; narrowed or pencil-shaped stools; blood or mucus in stool
Rectum: urgent need to defecate on awakening; alternating constipation and diarrhea; sensation of rectal fullness; dull ache in rectum/sacral region

Answer 123

A

Autosomal recessive condition found mainly in children and young adults
α1-antitrypsin is an enzyme inhibitor found in many tissues.
Normally prevents elastase and collagenase from damaging tissues
Genetically controlled by a gene with many allelic variations

Answer 124

A

•Defective α1-antitrypsin protein accumulates in liver; produces diagnostic granules

large amounts of abnormal alpha-1 antitrypsin protein (AAT) are made in the liver; nearly 85 percent of this protein gets stuck in the liver. If the liver cannot break down the abnormal protein, the liver gradually gets damaged and scarred.es.

Answer 125

A

Clinical manifestations

Centrilobular emphysema
Pancreatic insufficiency
Cirrhosis symptoms

Answer 126

A

•Peripheral neurons may regenerate if Schwann cells provide a pathway for growth.•Injury in PNS results in degeneration of the distal segment

Answer 127

A

•Neural stem cells in the ventricles and hippocampus can proliferate to produce glial or neuronal cells depending on specific cues.

Answer 128

A

Touch, pressure, and vibration travel up the ipsilateral side of the cord until the medulla
Pain, itch, and temperature usually cross over and travel to the brain on the contralateral side.

Intensity of the stimulus is reflected in the rate of action potentials generated

Answer 129

A

•Two major tracts

Dorsal column–medial lemniscal tract: fine touch, vibration, and proprioception•
Anterolateral tract: pain, temperature, and itch

•Sensory information from both tracts is transmitted from the thalamus to the same areas of the somatosensory cortex by way of the internal capsule.

Answer 130

A

•Requires interaction among the basal ganglia, cerebellum, and cortex•

Transmitted from the primary motor cortex down the corticospinal tract

Controls distal muscles of the arms, wrists, fingers, lower legs, feet, and toes
These are the muscles capable of fine-motor control

Answer 131

A

•Decussates in the medullary pyramids and travels down the spinal cord to control muscles on the contralateral side of the body

Answer 132

A

Geriatric considerations

Decreased cerebral blood flow, number of neurons, synthesis and metabolism of neurotransmitters, degeneration of myelin sheath and astrocytes, white and grey matter
Excessive degeneration of neurons – Alzheimer’s or senile dementia
Cerebral Atrophy
Dendrites shrink - slow cognition
Degeneration of myelin sheath - decreased reaction time.
Decreased neurotransmitters - tremors

Answer 133

A

Pathogenesis

•Excess CSF accumulation resulting in dilation of ventricles and compression of the brain and blood vessels due to ICP

Risk Factors

Premature birth, CNS tumors, CNS infections, cerebral hemorrhage, head injury
Congenital – primary cause – myelomeningocele
60% fatality rate if untreated

Clinical Manifestations

Infants with unfused cranial sutures
Unusually large head, bulging fontanelle, vomiting, dilated scalp veins, lethargy, etc.

Answer 134

A

Presents like Dementia or Alztimers - Slow process

Gait dysfunction, cognitive impairment, and urinary incontinence
Gait – wide stance and small steps
Cognitive – difficulty conceptualizing – slower psychomotor, decreased attention, apathy
Urinary – Urgency and incontinence

Answer 135

A

A Neural Tube defect where vertebrae does not fuse allowing the meninges and spinal cord herniation

Related to Folate Deficiency in pregnancy

Answer 136

A

Clinical manifestations

Spina bifida occulta – mildest, common

No protrusion of the cord, no symptoms
Sacral dimple , tuft of hair

Meningocele – rare

Meninges protrusion – sac on the back
No impairment

Myelomeningocele – open; most severe

Meninges, spinal cord, and nerves protrude
Paralysis, bowel and bladder dysfunction, seizures

Answer 137

A

Pathogenesis

Permanent, nonprogressive motor movement and muscle coordination
Cognition and communication dysfunction
Results from brain abnormalities or damage to cerebellum in prenatal period (childbirth)

•Risk factors

Male, African American, Low socioeconomic
Prematurity, LBW, breech births, multiple fetuses, hypoxia, hypoglycemia
Maternal smoking and alcohol use
Rubella or varicella during pregnancy

Answer 138

A

Classified according to movement disorder involved (area of brain affected)

Neurobehavioral signs - irritability
Developmental reflexes – exaggerated Moro reflex
Motor tone - varies from stiff to flaccid; delayed milestones
Spastic subtype - hyperreflexia; impaired fine motor skills
Dyskinetic subtype – irregular, unpredictable contractions of muscles
Ataxic subtype - uncoordinated movements, slow speech

Answer 139

A

Complications

Balance and coordination
Communication delays
Cognitive difficulties
Seizures
Vision and hearing deficits

Answer 140

A

Meninges - Meningitis

Brain parenchyma - Encephalitis

Answer 141

A

Inflammation of the meninges with inflammatory exudate causing obstructive hydrocephalus
Bacteria - Streptococcus pneumoniae; Neisseria meningitides; Haemophilus influenzae
Viral - West Nile, Influenza, HIV, herpes (aseptic)
Fungal or parasitic
Transmission modes – respiratory secretions, saliva, fecal-oral, insect bite, skull fracture

Answer 142

A

•Meningococcal vaccine - age 11-12 and booster at 16; Meningococcal B vaccine

HIB vaccine for infants

Answer 143

A

Clinical manifestations – mild to life-threatening

Mimic influenza infection – fever, chills, fatigue
Mental status changes
Nuccal rigidity
Severe headache
Kernig’s and Brudzinski’s sign

Answer 144

A

Brudzinski’s sign

Flex neck with chin to the sternum and the hips flex more than they were

Answer 145

A

Kernig’s sign

Flex knee and hip at 90 degrees and straightening the knee will cause lumbar pain

Answer 146

A

Pathogenesis

Brain inflammation, usually from viral infection
Viral - Coxsackievirus, Adenovirus; HSV-1;CMV; Equine virus, West Nile virus; measles, mumps
Bacterial – Lyme , TB, syphilis
Non-infectious – allergic reaction to vaccine
Transmission – respiratory droplets, insect bite,

Answer 147

A

Clinical Manifestations

Flulike symptoms – more gradual than meningitis
Headache
Nuccal rigidity
Confusion
Visual changes
Seizures

Answer 148

A

Pathogenesis

Flavivirus transmitted primarily by mosquitoes
Transmission from mother-fetus, sexual contact, blood transfusion

Clinical Manifestations

Flulike symptoms
Rash
Fatigue
Headache

Complications

Miscarriage
Microcephaly
Guillain-Barre

Diagnois with Zika Virus AB IgM in body fluid

Answer 149

A

Primary brain injury occurs as a direct result of the initial insult (Gunshot injury)

Secondary injury refers to progressive damage resulting from the body’s physiologic response to the initial insult. (hemorrhage)

Decreased ATP due to ischemia and hypxia leads to neuronal cell necrosis

Answer 150

A

Result of initial trauma/injury on brain cells

Focal injuries (coup) localized to site of impact
Polar injuries (coup contrecoup) caused by acceleration-deceleration movement of the brain within the skull, resulting in double injury (usually opposite focal injury)

Answer 151

A

•Diffuse injury caused by movement of the brain within the skull, resulting in widespread axonal injury. (Comatose)

Answer 152

A

•Eyes, Verbal response, Motor response

Mild – 13-15; Moderate 9-12; Severe <8

Answer 153

A

Cushing reflex – increased Systolic BP decreased Diastolic BP (widening pulse pressure); bradycardia, and Cheyne-Stokes respirations

•Baroreceptors detect HTN and trigger PNS to cause bradycardia; brain tissue pressure triggers respirations

Quick symptoms, Decreased LOC, Strokes, Trauma, Tumors

Answer 154

A

Clinical Manifestations

Decreasing level of consciousness
Vomiting
HTN, bradycardia
Papilledema, fixed and dilated pupils
Posturing, seizures

Answer 155

A

Mild traumatic brain injury; most common injury
Alteration or loss of consciousness (<30 minutes) but no evidence of brain damage on CT
Headache, nausea, vomiting, dizziness, fatigue, blurred vision, cognitive, and emotional disturbances

Answer 156

A

•Contusion: CT or MRI reveals an area of brain tissue damage (necrosis, laceration, bruising)

Answer 157

A

Classified by location
Epidural – Dura and skull involves arteries fast
Subdural – Dura and Arachnoid can take weeks esp with elderly
Intracerebral – into brain tissue
Subarachnoid – Arachnoid and pia mater worst HA of life back of head, aneurysm, arteriovenous maliformation

Answer 158

A

Collection of blood between the dura and skull

Rapid onset b/c it involves arteries

Significant deterioration of consciousness usually involves

skull fracture

Answer 159

A

Collection of blood between dura and outer layer of arachnoid membrane

Typically involves bridging veins

Symptom onset may be slower

Acute: symptoms within 24 hours of injury
Headache, vomiting, decline to coma
Subacute: symptoms develop 2-10 days after injury
Headache, vomiting, blurred vision
Chronic: symptoms develop 2 weeks or more after the injury

Answer 160

A

Collection of blood between arachnoid membrane and the pia mater
More commonly associated with rupture of cerebral aneurysms or arteriovenous malformations; arterial in origin
Blood spreads throughout CSF, causing meningeal irritation, hydrocephalus

WORST H/A OF LIFE IN

BACK OF HEAD

Answer 161

A

Bleeding into the brain tissue

Caused from HTN or contusions

HA, Vomiting, Seizure, Unilateral Weakness

Answer 162

A

Quadriplegic

Answer 163

A

Paraplegia

Answer 164

A

Interruption of cerebral blood supply leading to necrosis of specified area of brain tissue

Ischemic or hemorrhagic types

Answer 165

A

Risk Factors

Males affected more often than females
AA more than Caucasians
Risk factors - hypertension, DM, hyperlipidemia, smoking, advancing age, family history
Presence of carotid bruits

Answer 166

A

Pathogenesis

•Sudden occlusion of cerebral artery secondary to thrombus formation or emboli

Answer 167

A

Associated with atherosclerosis and coagulopathies

Answer 168

A

Associated with cardiac dysfunction or dysrhythmias (atrial fibrillation)

Answer 169

A

Small penetrating infarcts need MRI to diagnose

Answer 170

A

F—Face: Ask the person to smile. Does one side of the face droop?
A—Arms: Ask the person to raise both arms. Does one arm drift downward?
S—Speech: Ask the person to repeat a simple phrase. Is the speech slurred or strange?
T—Time: If you see any of these signs, call 9-1-1 right away.

Answer 171

A

•Neurologic symptoms typically last only minutes, but they may last as long as 24 hours.

Symptoms resolve completely without evidence of neurologic dysfunction

Answer 172

A

Hemorrhage within the brain parenchyma
Usually occurs secondary to severe, chronic hypertension
Most occur in basal ganglia or thalamus

Hemorrhagic Stroke is worse than Ischemic due to area affected

Answer 173

A

Initially, motor deficits occur; flaccidity or paralysis with recovery occurring with onset of spasticity, contralaterally to the side of the brain where the stroke occurred

Sensory disturbances occur in same locations as motor paralysis

Answer 174

A

Homonymous hemianopsia, the same side of the retina in each eye is blinded

Answer 175

A

Broca aphasia (verbal, motor/expressive) poor articulation and sparse vocabulary

Aphasia occurs with brain damage to the dominant cerebral hemisphere and can involve all language modalities.

Answer 176

A

Wernicke aphasia (sensory, acoustic, receptive)

impaired auditory comprehension and speech that is fluent but does not make sense

Aphasia occurs with brain damage to the dominant cerebral hemisphere and can involve all language modalities

Answer 177

A

Lesion of an artery that results in dilation and ballooning of a segment of the vessel
Congenital defect of the medial layer of the artery weakens, allowing dilated portion to fill with blood and eventually burst causing hemorrhage; most found in circle of Willis

Answer 178

A

Risk Factors

•HTN, acute alcohol intoxication, and recreational drug use (especially cocaine) implicated

Clinical Manifestations

Severe Headache
Photophobia
Nausea/vomiting
Rapid decline in status

Answer 179

A

The capillary system fails to develop appropriately with arterial blood shunted directly into the venous system; causes the vessels to progressively enlarge; becomes a congested mass of enlarged vessels that can burst.

Answer 180

A

Seizure and neurologic dysfunction due to hemorrhage

Answer 181

A

Pathogenesis

Severe headaches as a result of neural depolarization across the cerebral cortex
Activate trigeminal nerve
Inflammation of cerebral vessels
Release of calcitonin gene-related peptide (CGRP) causing cerebral vessel vasodilation

Answer 182

A

•Prodrome – 1-2 days before

Irritability, euphoria, depression yawning, food craving, constipation

•Aura – precedes headache

Partial visual changes, loss of speech, sensory, language, and motor auras

•Migraine

Throbbing or pulsatile pain – unilateral and can last hours or days
Nausea and vomiting
Photophobia and phonophobia

•Postdrome

Fatigued

Answer 183

A

Migraine without aura

Minimum of 5 headache attacks that last between 4-72 hours in length

Headache attacks must include the following qualities:
Occur unilaterally - pulsatile
Pain that is moderate to severe in intensity
And/or aggravated by physical activity
Accompanied by: Nausea and/or vomiting, Photophobia, and/or phonophobia

Answer 184

A

Migraine with aura

Must have at least 2 headache attacks with aura including visual, sensory, and/or language symptoms

Two of the following must occur:

One of the aura symptoms must progress in intensity over a period of 5 minutes or greater
At least two of the above aura symptoms must occur one after another
A single aura symptom lasts from 5 to 60 minutes
One aura symptom occurs unilaterally
Headache occurs simultaneously with the aura
Headache begins within 60 minutes of the aura symptoms

Answer 185

A

Pathogenesis

•Result from hypersensitivity of nerve fibers

PNS and muscular hypersensitivity
Episodic or chronic
Men and women equally

•Clinical Manifestations

Dull, full, or tight feelings – nontrobbing
Bilateral
No aura or photophobia

Answer 186

A

Pathogenesis

Short bursts of intense unilateral orbital pain due to activation of the trigeminal nerve
Men more than women

Clinical Manifestation

Trigeminal distribution of the pain
Unilateral and same side autonomic features
Severe throbbing or stabbing pain lasting minutes to hours
Lacrimation, ptosis, pupil constriction

Answer 187

A

•Provoked – brain trauma, hematomas, hypoglycemia, infection, chemicals

Unprovoked - epilepsy

Answer 188

A

Conscious with unexplained mood change
Sensory change – hear, smell, see

Answer 189

A

Complex focal

Change in consciousness and memory
Repetitious behaviors – blinking, twitching
Aura

Answer 190

A

Generalized seizures

Absence – petit mal; starring <15 seconds
Myoclonic – jerking of upper or lower body
Atonic – drop due to loss of muscle tone
Tonic-clonic – grand mal; LOC, jerking, post-ictal

Answer 191

A

Pathogenesis

Chronic demyelinating disease of the CNS that primarily affects young adults
Autoimmune disorder that results in inflammation and scarring (sclerosis) of myelin sheaths covering nerves (T cells); Cytokines

Answer 192

A

•Demyelination can occur throughout the CNS but often affects the optic and oculomotor nerves and spinal nerve tracts.

Answer 193

A

•Female; Vitamin D deficiency; EBV

Answer 194

A

Clinical Manifestations:

Double/blurred vision, weakness, poor coordination, and sensory deficits; bowel and bladder control may be lost; memory impairment common
Marked by exacerbations and remissions; exacerbated by heat, infection, trauma, stress

Answer 195

A

Progressing-Relapsing MS

Second Progressive MS

Primary-Progressive MS

Relapsing-Remitting MS

Answer 196

A

Pathogenesis

May be idiopathic, acquired or drugs
Dopamine deficiency in the basal ganglia (substantia nigra) associated with motor impairment
Lewy Bodies – clumped proteins in neurons

•

Answer 197

A

•Incidence

More males than females
Average age – 65
Diagnosis to death – 15 years

•Risk Factors:

Head trauma
Environmental toxins
Family history

Answer 198

A

Clinical Manifestations

•General lack of movement
•Loss of facial expression
•Propulsive (shuffling) gait with absent arm swing

•Difficulty initiating and controlling movements:

•Akinesia – absence of movement
•Bradykinesia – slow movement
•Tremor - at rest; pill-rolling movement
•Rigidity - cogwheel rigidity
•Micrographia

•Mood and cognition changes

Answer 199

A

Diagnosis

History and examination
Bradykinesia with tremor or rigidity
CT/MRI Brain
CBC, CMP

Answer 200

A

Parkinson Stooped Posture Progression

Answer 201

A

Pathogenesis
Genetic mutation – autosomal dominant
Involuntary movement of a body part - hand or head

Answer 202

A

•Clinical Manifestations

Action Tremor - worsens with activity
No rigidity of extremities
Usually bilateral
Macrographia

Answer 203

A

Pathogenesis:

Acute idiopathic paralysis of the CN VII facial nerve - unilateral

Etiology:

Inflammatory; Compression; Viral (Herpes Simplex)

Answer 204

A

Clinical Manifestations:

Rapid onset - 24-48 hrs
Diminished eye blink
Hyperacusis - reduced tolerance to sound
Decreased lacrimation
Uneven smile
Uneven eyebrow lift - cannot raise eyebrow flat forehead
Facial sensation usually intact

Answer 205

A

Pathogenesis

Damage to motor neurons of cerebral cortex, brain stem, and spinal cord
Spinal cord atrophy resulting in muscle atrophy
Continuous and rapid decline in motor function
Exact etiology is unknown, genetic mutation or autoimmune
Onset > age 45; family history; men> women

Answer 206

A

•Clinical manifestations

Spinal cord injury leads to Footdrop, weakness and eventual wasting (atrophy) of upper or lower extremities; dysarthria or dysphagia, respiratory dysfunction leads to death

•Diagnosis:

History and examination; no definitive test
MRI Brain; Lumbar puncture
Electromyogram
No definitive test

Answer 207

A

Syndrome associated with many pathologies; characterized by progressive deterioration and continuing decline of memory and other cognitive changes

Not to be confused with delirium

Abrupt onset may fluctuate often, becoming worse at night; disturbed consciousness, decreased awareness of the environment, incoherence, and hallucinations.

Types

Alzheimer: most common
Vascular

Answer 208

A

Pathogenesis

Degeneration of neurons in temporal and frontal lobes, brain atrophy, amyloid plaques, and neurofibrillary tangles
Deficient synthesis of brain acetylcholine
Cause remains unknown, although genetic factors (family history increases 4x) and environmental triggers suspected
Aging increases risk

Answer 209

A

Clinical Manifestations

Behavioral problems progress from forgetfulness to total inability for self-care
Depression and psychosis may be significant
Language and balance decline
Problem solving, loss of judgement

Answer 210

A

Pathogenesis

Progressive loss of cerebral function from single cerebrovascular insults
Risk factors: CVA or lacunar stroke, hypertension, diabetes, smoking

Answer 211

A

Clinical manifestations

•Memory loss, especially short-term memory, long-term memory may be preserved; Cognitive thinking ability declines, decreasing ability to function at work and in social settings; anxiety, agitation

Diagnosis is same as Alzheimers except no genetic testing

Answer 212

A

Pathogenesis

Formation of Lewy bodies
Made of proteins ubiquitin and synuclein
Decreased dopamine and cholinergic neurons
Genetic mutation

Answer 213

A

Clinical Manifestations

•Progressive dementia

Early impairment of attention, executive and visuospatial functioning, cognitive fluctuations
Daytime somnolence
Visual hallucinations
Parkinson features

Answer 214

A

Pathogenesis

Focal degeneration of frontal and/or temporal lobes
Motor neuron disorder similar to ALS

•Clinical manifestations

Behavioral variant - progressive personality and behavioral changes, impulsivity
Nonfluent – expressive (motor) language deficits
Semantic – difficulty understanding words

Impulsive and NO Amyloid Plaques

Answer 215

A

Life-threatening whether malignant or benign – space occupying lesion
Cause increase in ICP and resulting symptoms
Primary vs. secondary tumors

Answer 216

A

Pathogenesis

Mood disorder commonly featuring persistent sad, empty, or irritable mood
Genetic factors – chromosome alteration with bipolar, schizophrenia, spectrum disorders, ADHD
Hypothalamus-pituitary axis – cortisol and growth hormone
Abnormal neurotransmitter functioning
Serotonin – mood, cognition, anxiety
Norepinephrine - mood, attention
Dopamine - pleasure and pain
GABA - anxiety
Acetylcholine - learning and memory
Life Events

Answer 217

A

Major depressive disorder (MDD) (5 symptoms)

Sad, empty, hopeless, loss of interest
Changes in weight, sleep, and activity
Fatigue
Diminished ability to concentrate or indecisiveness
Impaired functioning

Answer 218

A

Persistent depressive disorder

Same as MDD but present most days for 2 years

Premenstrual dysphoric disorder

Symptoms present one week before menses
Impact work and social function

Answer 219

A

Diagnosis

History and physical exam
CMP, CBC, TSH
DSM-V criteria
Tools - PHQ-9 - depression
Mood Disorder Questionnaire – Bipolar
GAD-7 – anxiety

Answer 220

A

Mania for at least one week alternating with episodes of MDD

Answer 221

A

Hypomanic episode of 4 day duration alternating with MDD symptoms

Answer 222

A

4 or more episodes of alternating moods in a year

Answer 223

A

Pathogenesis

Genetic link

Neurotransmitter abnormality – serotonin, norepinephrine, GABA, dopamine

Most prevalent mental health disorder

Types of anxiety disorders

Panic Disorder

Generalized Anxiety Disorder

Social Anxiety Disorder

Answer 224

A

Panic disorder – unexpected abrupt intense fear (perpetual)

Palpitations, diaphoresis, chest pain, dizziness

Answer 225

A

Generalized anxiety disorder – excessive worrying about life events

Present most days; less than 6 months
Restless, insomnia, fatigue

Answer 226

A

Social anxiety disorder – fear or anxiety in social situations to the point of avoiding them

Present more than 6 months
Significant impairment in the situation

Answer 227

A

Bone to Bone

Answer 228

A

Muscle to bone

Answer 229

A

Pathogenesis
Abnormal acetabular and proximal femur development which may not be totally present at birth. Resulting in abnormal shape of the acetabulum

Risk factors

Females 3 x more likely than males
Breech position

Answer 230

A

Clinical manifestations

Partially or fully dislocated – unilateral or bilateral. Left more than right
Less than 12 months
Hip instability, asymmetric leg creases, limited hip abduction
Older than 12 months with walking
Altered gait, excessive lordosis (curvature of the lumbar spine), Genu Valgum (knocked knee’d) acetabulum

Answer 231

A

Pathogenesis
Rare connective tissue disorder resulting in fragile bones and fractures

Autosomal dominant disorder with mutation of collagen genes causing lax ligaments

Answer 232

A

Clinical manifestations

Excessive and atypical fractures (child abuse suspected)

May have short stature and limbs

Hearing loss

Premature osteoporosis

Answer 233

A

•Kyphosis - thoracic spine curved outward (hump)

Scheuermann - juvenile development during adolescent growth spurt; pain with activity

Adult – degeneration of vertebrae, osteoporosis, fracture; back pain, spine stiffness

Answer 234

A

•Lordosis – exaggerated concave lumbar spine

Develops in adolescent with poor posture; worsens with pregnancy and obesity; low back pain

Answer 235

A

•Scoliosis – lateral deviation or rotation of thoracic or lumbar spine resulting in asymmetrical hip and shoulder alignment, thoracic cage or gait; back pain, respiratory compromise

Uneven hip height

Answer 236

A

•Comminuted fracture: more than one fracture line and more than two bone fragments

Answer 237

A

•Nondisplaced fracture: fragments remain in alignment and position; displaced: ends of fracture fragments are separated

Answer 238

A

•Depressed fracture: fragment displaced below the level of the bone surface

Face or Skull is common

Answer 239

A

2 view plain x-ray

AP/LAT

Repeat x-ray in 1-2 weeks if fx is suspected but not easily seen due to swelling

Answer 240

A

•Delayed union

Anywhere from 3 to 6 months after the fracture, bone pain and tenderness are continuously increasing beyond the expected healing period.

Answer 241

A

•Malunion

Healed fine but Improper alignment of fracture fragments often if untreated this results

•Nonunion

Not healed by >6 months after a fracture, can use bone stimulator to regrow bone

Answer 242

A

Pathogenesis

Severe pyogenic infection of bone and local tissue; staph aureus or group A strep
Organisms reach bone through bloodstream, adjacent soft tissue or direct introduction of organism into bone causing necrosis
Adjacent soft tissue: Caused by to burns, pressure ulceration, trauma, periodontal infection
Direct infection causes open fracture, penetrating wounds, surgical contamination, or insertion of prostheses, metal plates, or screws

Answer 243

A

Clinical Manifestation

•Pain in joint or tenderness
•Swelling
•Erythema and warmth
•Fever if systemic

Diagnosis

CBC, ESR and CRP

Answer 244

A

Pathogenesis
Death of bone tissue due to loss of blood supply to the bone directly – bone dies
Trauma, dislocation, fracture
Steroid use or alcoholism

Often affects hip joint, pain with activity

Answer 245

A

•Pathogenesis

Separation of two bones at a joint
Subluxation is partial separation

•Clinical manifestations

Deformed or visible abnormal joint
Limited movement, swelling or bruising, intense pain

Answer 246

A

•Injury to a ligament when stretching exceeds ROM of the joint ; may result in partial to complete tear of the ligament structure

Answer 247

A

•Clinical manifestations

•Pain, joint stiffness, limited function, rapid swelling of the joint , difficulty bearing weight, discoloration due to bleeding and bruising
(Knee & labrum (medial meniscus) is most common)

Diagnosis with MRI to see soft tissue injury

Answer 248

A

•Pathogenesis

•Injury to muscle or tendon or joint of both due to overuse or awkward muscle movement
•Inflammation and bleeding at site of injury
•Decreased collagen elasticity with age
•Lumbar region is the most common

Answer 249

A

Clinical manifestations
Pain, stiffness, difficulty moving affected muscle, edema

BRUISING

Diagnosis with MRI and US

Answer 250

A

•De Quervain’s Tendonitis - thumb radial head to tip of thumb – cant open jar

Answer 251

A

•Bicep tendonitis – upper arm/anterior shoulder – no pain on lifting arm pain curling arm

Answer 252

A

Pathogenesis

Inflammation of fluid-filled, pocket of connective tissue between muscles or between muscle, tendon, and bone due to trauma or overuse
Bursea contain synovium to cushion the structures

Olecranon, trochanter, patellar

Answer 253

A

Types

Acute bursitis – sudden pain with flexion of the joint, swelling
Chronic bursitis – gradually develops, less painful
Septic bursitis – infection, erythema, swelling, warmth – would not have with reg bursitis only septic

Answer 254

A

Idiopathic loss of active and passive range of motion (inflammatory/fibrosing)
Can occur from prolonged immobilization
Manifestations - severe, diffuse pain, loss of ROM (you or the patient cannot move shoulder)
Diagnosis - Examination; MRI

Often after a fall and arm is in slin too long pt loses ROM and literally arm cannot be moved have to go under anesthesia to break up scar tissue

Answer 255

A

•Shoulder impingement syndrome

•Compression of structures around glenohumeral joint with shoulder elevation
•Development from repetitive work or sports activities causing edema, fibrosis, and tendonitis
•Manifestations – pain with arm above shoulder or lying on it - Pain happens when you elevate it
•Diagnosis – examination, MRI

Answer 256

A

Pathogenesis

•Tendinopathy of tendon just distal and anterior to epicondyle due to thickened and scarred tendon

Answer 257

A

Clinical Manifestations

•Lateral (more common) on radial side - thumb

•Pain in lateral elbow and forearm with gripping or wrist extension

•Medial ulnar side - pinky (golfers hand)

•Pain in the medial elbow with wrist flexion and forearm pronation

Treatment is rest

Answer 258

A

Carpal tunnel syndrome

Compression of median nerve in the carpal tunnel from anatomic position or inflammation
Manifestation - pain or paresthesia with wrist flexion, worse at night; 1-3 fingers radially

Diagnosis – examination – Tinel or Phalen test; nerve conduction study

Answer 259

A

de Quervain tendinopathy

•Inflammation of wrist tendons on radial side
•Manifestation - swelling and pain on distal radial side and with movement of the thumb
•Diagnosis – examination
Finkelstein test

Answer 260

A

Phalen Test for Carpal Tunnel Syndrome

Answer 261

A

•Dupuytren’s contracture

Thickening and contracture of the palmar fascia due to fibroblast proliferation and abnormal collagen deposition
Manifestation – limited extension of the finger

Answer 262

A

•Trigger finger

Abnormal thickening of flexor tendon at the metacarpophalangeal joint
Manifestation - pain and “catching” with flexing

Answer 263

A

•Slipped capital femoral epiphyses

•Common cause of hip pain in adolescents
•Femur head slipping backwards off neck of bones
•Manifestation – acute, dull hip pain, abnormal gait; decreased ROM
•Diagnosed – exam and hip x-rays walk with hip/leg flexed outward

Rotate foot out when walking

Answer 264

A

Meralgia paresthetica

Mechanical compression of nerve supplying sensation to upper, outer thigh (obesity) police officers and people with belts
Manifestation - burning pain, numbness, and tingling over outer thigh

Answer 265

A

•Pathogenesis

•Osteochondritis of tibial tubercle with patellar tendonitis
•Occurs in adolescents with rapid growth spurts
•Result of overuse injury, trauma in sports
•Repetitive strain and chronic avulsion

Answer 266

A

•Manifestation - anterior knee pain with squatting, jumping (ligaments pulling or pounding)

Answer 267

A

Mechanical - muscle strain, disc or facet joint degeneration, vertebral fractures, spinal stenosis
Nonmechanical - neoplasms, infections, multiple myeloma, metastatic cancer, ankylosing spondylitis, spondylolisthesis

Answer 268

A

•Radiculopathy – damage near the nerve root at the spine

Answer 269

A

LS spine X-rays; CT or MRI
Nerve conduction study, myelogram, electromyography

•

Answer 270

A

Poor body mechanics, obesity, heavy lifting, trauma, repetitive use; demineralization with osteoporosis

Answer 271

A

•Degenerative Disc Disease

Normal aging process with discs losing hydration and disc decreases height
Spondylosis – narrowed disc space or degeneration of the two facet joints

Answer 272

A

•Herniated Disc Disease

Gelatinous nucleus protrudes through the fibrous outer covering of the disc
Bulge or herniation can place pressure on the spinal cord and disrupt nerve conduction which may be permanent
Can be multilevel - cervical or lumbar

Answer 273

A

Pathogenesis

Narrowing of the spinal canal due to degeneration and spondylosis; RA
Ligamentum flavum can thicken
Causes mechanical compression and ischemia of nerve roots
Usually > 60 years old

Answer 274

A

•Manifestations

Pain with movement
Radicular pain – radiating pain, paresthesia, muscle weakness; decreased reflexes
Sciatic pain – injury at L5 or S1

Answer 275

A

•Compression of the lumbar and sacral nerve roots from herniated disc, tumor, or trauma

Manifestations

Low back pain with bilateral radiation into both legs
Motor weakness
Bowel and bladder dysfunction

Answer 276

A

•Pathogenesis

Progressive loss of bone strength due to low bone mass
Decrease in osteoblast or increase in osteoclast activities or both
Greater bone removal than building – RANKL binding
Increases risk for fracture

Answer 277

A

•Risk

Loss of estrogen and androgen
Women more than men
Caucasian and Asian
Over age 50
Diabetes; thyroid; Cushing, hyperparathyroid
Smoking
Poor calcium and Vitamin D intake
Disuse
Alcohol use

Answer 278

A

Binds to osteoclasts (break down of bone) and increase resorption

Answer 279

A

•Manifestations

Asymptomatic until a fracture occurs
Vertebral fracture < 65 years of age
Hip fracture > 65 years of age
Kyphosis
Height reduction

Answer 280

A

•Diagnosis

Bone mineral density (BMD); measure by dual-energy x-ray absorptiometry (DXA)
Osteoporosis: T score < −2.5;
Osteopenia: T score between −1.0 and −2.4
CMP, Vitamin D, TSH

Answer 281

A

Rickets

Softening and weakening of bones
Extreme and prolonged vitamin D, calcium, or phosphate deficiency

Osteomalacia

Deficient mineralization affecting the bone matrix

•Manifestations

Bowed legs, Scoliosis
Fractures
Bone pain

Answer 282

A

•Pathogenesis

Abnormal bone destruction and remodeling resulting in bone deformities
Bone turnover 20 times faster than normal
Develop weakened and deformed bones
Genetic or viral cause

RAPID TURNOVER OF WEAK BONE

Answer 283

A

•Clinical manifestations

•Asymptomatic in early disease
•Bone pain, skeletal deformities, fractures, neck pain, hypercalcemia, lytic lesions
HYPERCALCEMIA

Answer 284

A

Pathogenesis
Local degenerative joint disorder associated with aging and wear and tear from repetitive stress, deterioration of cartilage causing bone friction
Progressive, non-inflammatory disease of diarthrodial joints (movement/weight bearing joints)
Results in loss of articular cartilage, cartilage calcifies, wear of underlying bone, and the formation of bone spurs

Answer 285

A

•Manifestations

Localized joint pain and crepitus with movement
Bony enlargement, morning stiffness lasting < 30 minutes or after inactivity
Heberden and Bouchard nodes (buttons on distal joints)

Answer 286

A

Systemic autoimmune inflammatory disease

Pathogenesis:

T and B cells are activated; B cells escalate the inflammatory response
B cells produce RF antibodies against IgG and anti-CCP antibodies
Inflammatory response in rheumatoid joint leads to accumulation of immune cells and infiltration of the synovium.
Granulation tissue forms over articular cartilage causing erosion and destruction of articular cartilage, resulting in bone erosion, bone cysts, and fissures.
Genetically predisposed individuals

Answer 287

A

Manifestation

Classic presentation: bilateral symmetric polyarthritis involving smaller joints
Morning stiffness for more than 1 hour, pain at rest
Aching joint pain worse with movement or pressure
Joint swelling and eventual deformity
DIP joints are usually spared
Swan neck appearance of hands

Answer 288

A

Diagnosis

History and examination
X-rays, MRI
Rheumatoid Factor (RF) elevation
Anti- CCP elevation –more specific test
ESR and CRP elevation
Synovial fluid aspiration

Answer 289

A

Category of childhood arthritis

No relationship to seropositive rheumatoid arthritis
Psoriatic, Oligoarthritis (4 or less joints), Polyarthritis (5 or more joints), Systemic
Major clinical manifestations
Synovial thickening and fluid accumulation
Diagnosis and treatment similar to other arthritis forms

Answer 290

A

Pathogenesis

Inflammatory disease from deposits of uric acid crystals due to overproduction or undersecretion of uric acid
Tophi develop over time
Uric acid produced with breakdown of purines

Answer 291

A

•Risk Factors

Males more than females
Obesity
Alcohol
Medications – thiazide and loop diuretics

Answer 292

A

Clinical manifestations

Rapid onset of pain at affected joint (lower extremity), joint warmth, redness, swelling
Renal calculi

Answer 293

A

Pathogenesis

Progressive inflammatory disorder affecting sacroiliac joints, intervertebral spaces, and costovertebral joints
Inflammation leads to destruction of the joint and fibrosis and calcification causes fusion
Age 20-40; males > females

DOESN’T GET BETTER WITH REST

Answer 294

A

Clinical manifestations

Five characteristics

<40 years old
Insidious onset
Improves with exercise
No improvement with rest
Pain worst at night and better with rising

KYPHOSIS AND LOSS OF LUMBAR LORDOSIS

(BACK FUSES STRAIGHT)

Answer 295

A

Pathogenesis

Inherited, non-inflammatory disorders characterized by skeletal muscle degeneration

Nine different forms

Duchenne MD – most severe, most common affecting only males

Answer 296

A

Clinical manifestations
Intellectual disability, muscle weakness, muscle spasms, poor coordination, delayed motor skills

DIAGNOSE WITH MUSCLE BIOPSY

Answer 297

A

Pathogenesis

•Cause remains unknown; possible central sensitization – amplification of pain fiber impulses

Manifestation

Widespread pain and muscle tenderness for 3 months
Fatigue, insomnia, depression, and concentration problems
Tender/trigger points
Diagnosis

Rule out all other causes

Answer 298

A

Chronic multisystem, inflammatory, autoimmune disease characterized by periods of exacerbations and remission
Considered an atypical inflammatory reaction to the body’s own tissues, cells, and protein
Overactive B-lymphocytes → overproduction of autoantibodies and ↑ reactivity of T-lymphocytes

Peak incidence 15 to 40 yr olds

Affects collagen tissue

Renal impairment, heart disease and infection

Answer 299

A

ANA Qualitative screen - + or –
ANA Quantitative - ratio result

1:40 or greater is positive

•ANA with reflex : Anti-SM

Anti -dsDNA

Answer 300

A

•Multisystem inflammatory connective tissue disease characterized by skin thickening and deposition of collagenous tissue resulting in severe fibrosis of unknown cause

Answer 301

A

Manifestations:

Raynaud phenomenon (white fingertips), polyarthritis, sclerodactyly, macular rash, and internal organ involvement
Pulmonary fibrosis; CHF; Renal Crisis with malignant HTN

Answer 302

A

Commonly called Charcot joint

Pathogenesis
Bone and joint abnormalities caused by loss in normal position sense and pain responses
Most commonly caused by diabetes
Manifestation – seen in diabetic patients
Swollen, deformed, and unstable joint

Answer 303

A

Pathogenesis

Progressive motor and/or sensory nerve damage
Feet and legs first, then hands
Decreased strength as well as sensitivity
Hereditary: autosomal dominant or recessive

•Manifestation

Can develop foot drop and decreased use of extremities
Paresthesia of extremities

Answer 304

A

Osteosarcoma

Extremely malignant bone-forming tumor and most common
Formation of bone or osteoid by tumor cells
Occurs in children and young adults
Located in distal end of the femur, proximal end of the tibia, fibula, humerus and flat bones of the pelvis, skull, scapula, ribs, or spine
Rapid development

Answer 305

A

Chondrosarcoma

Malignant cartilage-forming tumor that develops slowly; tends to develop in the pelvic and shoulder girdles and the proximal ends of long bones
Characterized by formation of cartilage by tumor cells
Occurs in those 30 to 60 years of age

Answer 306

A

Ewing Sarcoma

Third most common primary sarcoma; rapidly growing malignant round cell tumor
Develops in the long bones between 5 to 25 years of age
Metastasizes quickly to other bone and lung
Pain is a dominant symptom and appears systemically ill

Answer 307

A

Keratinocytes

Answer 308

A

Melanocytes

Answer 309

A

adipose cells

Answer 310

A

blood vessels

Answer 311

A

fibroblasts

Answer 312

A

Hypopigmentation areas from melanocyte death or melanin formation loss
All skin tones but more noticeable with dark skin tone
Etiology:
Autoimmune condition, genetic influences, sunburn, and emotional stress
Age range 10-30 years at presentation
Manifestation patterns
Nonsegmental
Focal (localized) or generalized (widespread)

Segmental – one side of the body

Answer 313

A

Young children and elderly = less fx sweat glands and are less efficient evaporative heat loss capabilities

Sebaceous glands more active during puberty

Sebaceous glands less active with age = dry skin

Answer 314

A

Proliferative/neoplastic
Proliferative conditions include psoriasis, seborrheic keratosis, cysts, warts, and papillomas
Benign skin growths
Skin cancer is the most common malignancy in the United States

Answer 315

A

Etiology - Cutaneous reaction to topical irritation from chemicals

Pathogenesis

Irritant is inflammatory response in <24 hours
Presentation:
Erythema
Edema
Lesions – vesicles or blisters
Puritis
Scaling or necrosis with prolonged exposure

Answer 316

A

Etiology - Cutaneous reaction to allergen substance - metals, plants, chemicals

Pathogenesis

Allergic is Type IV hypersensitivity response in 48-72 hours
Presentation: at the site of contact
Puritis
Erythema
Edema

Lesions – vesicles or bullae

Answer 317

A

•Chronic inflammatory condition – eczema

Etiology - Inherited tendency; family hx of eczema, asthma

•More common in children

Pathogenesis - immune system malfunction

Manifestations
Xerosis and pruritus
Face, scalp, extensor surfaces (knees, elbows)
Diagnosis
History and physical exam
Elevated IGE level

Answer 318

A

Papulosquamous skin disease manifested by various degrees of scaling and erythema in areas of high oil gland concentration
Cradle cap (infants) and dandruff (adults)
Facial area

Answer 319

A

Etiology – allergic food or medication exposure
Pathogenesis –
Histamine release initiated by various substances
Types I, II, and III hypersensitivity
Manifestation
Circumcised erythematous plaques, blanchable
Intensely pruritic

Answer 320

A

Cutaneous reactions to medication usually begin within 1 week of exposure.
Most common eruption is an erythematous maculopapular rash, usually widespread.
Severe cases involve erythema multiforme (including Stevens-Johnson syndrome).

Answer 321

A

Chronic inflammatory condition

Etiology - Inherited condition; immune system involvement; Adult condition

Pathogenesis - Inflammation promotes hyperproliferation of the skin

Triggers – cold weather, stress, alcohol
Manifestations – Chronic plaque presentation
Papules and plaques with overlying silvery scale

•Lesions on knees, elbows, lower back, scalp, nails

•Joint pain with psoriatic arthritis

Exacerbation and remission

Answer 322

A

•Folliculitis – hair follicles

•Tender pustules in areas of hair

•Furuncles – boils

•Firm, erythematous, painful nodule with purulent exudate

•Impetigo (non-bullous and bullous)

•Caused by staphylococci or streptococci bacteria
•Characterized by vesicles, pustules, and yellowish crusts

Answer 323

A

Infection deep into dermis and SQ layer
Localized warm, tender, erythematous area
Systemic fever, leukocytosis

Answer 324

A

•Necrotizing fasciitis

•Rare but high mortality
•Aggressively destroys skin, fat, muscle due to toxins released
•Rapidly worsening infection with systemic manifestations
•Gram + Streptococcus A

Answer 325

A

•Two types infect the skin

•HSV-1 occurs above the waist; common on the lips, face, and mouth; pain common, healing in 10 to 14 days; persists in latent form.
•HSV-2 responsible for most infections in genital area
•Usually begin with a burning or tingling sensation followed by vesicles and erythema; crusts before healing
Ocular involvement can lead to blindness
Remains dormant in dermatome until next occurrence

Answer 326

A

Shingles: acute localized inflammatory disease of a dermatomal segment of the skin caused by varicella zoster (chickenpox)
Results from reactivation of the latent virus
Eruption of painful vesicles with erythematous bases; unilateral along a specific dermatome
Dormant in cranial or spinal nerve until the next occurrence

May cause a permanent neuropathic pain

Answer 327

A

Warts: common benign papillomas caused by DNA-containing papillomaviruses
Exaggeration of normal skin composition; stratum corneum irregularly thickened
May resolve spontaneously if immunity develops

•Types

•Verruca Vulgaris - common wart
•Verruca Plana – flat topped papules
•Verruca Plantaris - on plantar surface of the foot

Answer 328

A

Common in children
Spread with direct skin contact or contaminate object like a razor
Firm dome-shaped white papules with craterlike center

Answer 329

A

•Occurs after a viral infection

•Benign, uncommunicable

Starts with a herald patch – solitary, salmon colored well demarcated patch on chest, neck, or back
2-14 days later develop scaly papules and plaques in a Christmas tree pattern on the posterior trunk

Answer 330

A

•Infection (tinea) named after location:

Tinea corporis (trunk) - circular, erythematous scaling patch. Raised border and central clearing
Tinea capitis (scalp) - same as corporis with hair loss at site
Tinea barbae (beard)
Tinea manus (hand)
Tinea cruris (groin) – confluent erythema with vesicles or pustules
Tinea pedis (foot) - erythematous fissures or scales
Tinea unguium – yellowed nails, thickened

Answer 331

A

Benign, noncommunicable
Malassezia genus – normal flora
Prompted by heat, humidity, and excessive sweating
Occurs on the trunk and distal extremities
More prevalent in adolescents and young adults
Hypopigmented patches

Answer 332

A

Sarcoptes scabiei is a mite.
Begins with eggs laid in the stratum corneum, hatch into larvae within 3 to 4 days
Contracted after close contact with an infested individual
Small erythematous papules with overlying dry scale or crust; linear burrows
Finger webs; wrists, groin

Answer 333

A

Caused by tick that carries Rickettsia rickettsii; most states have reported cases
Initial bite appears as papule or macule with or without a central punctate area.
Within 4 to 8 days HA, fever, N/V, and muscle aches appear; macular, maculopapular rash on wrist/ankle

Answer 334

A

Tick bite that carries spirochete Borrelia burgdorferi from deer and mice
Affects skin, nervous, heart, and musculoskeletal system
Stage I: single or multiple erythematous papules that itch or sting; flulike symptoms
Stage II: meningitis, cranial nerve palsies, and peripheral neuropathy
Stage III: oligoarticular arthritis

Answer 335

A

Etiology

•Caused by contact with or exposure to extremes of temperature
•Dry heat: flames or hot surfaces
•Moist heat
•Hypothermia and frostbite: also thermal injuries
•Chemicals

Answer 336

A

Cellular Changes

Cell membrane transport defect related to alteration in the steady-state composition, characterized by high intracellular concentrations of sodium (sick cell syndrome)
Decrease in the efficiency of the sodium-potassium pump; diminished membrane potential (calcium channels disrupted); reversed with adequate fluid resuscitation

Answer 337

A

•Three zones of injury in burn wound

Zone of necrosis: area in the burn wound where coagulation necrosis has occurred
Zone of stasis: surrounds necrosis, decreased blood flow that is reversible with adequate resuscitation, if not adequate, will necrose
Zone of hyperemia: surrounds stasis, comprised of minimally injured tissue that usually recovers normal function

Answer 338

A

First degree (superficial)
Second degree (superficial and deep partial thickness)
Third degree (full thickness)
Fourth degree (full thickness with bone or muscle involvement)

Answer 339

A

First-Degree: Superficial Burns

Involve only superficial tissue destruction of outermost layers of the epidermis
Manifestations: local discomfort, erythema, headache, chills, N/V
NO BLISTER
Typically self-limiting, healing in 3 to 6 days

Answer 340

A

Second-Degree: Superficial Partial-Thickness Burns

Involve the epidermis to the level of the dermis and appear red to pale ivory
Moist thin-walled blisters often form
Pain is a major clinical feature.
Injuries typically heal in 7 to 21 days in the absence of wound infection.

Hair typically reappears in 7 to 10 days.

Answer 341

A

Second-Degree: Deep Partial-Thickness Burns

Involve entire dermis; leave only epidermal skin appendages (hair follicles)
Mottled appearance; large areas of waxy-white tissue surrounded by light pink or red tissue, blisters flat and dry
Heal in about 4 weeks
Treatment: usually excised early, skin grafts diminish scarring and promote early wound closure

Answer 342

A

Third Degree: Full-Thickness Burns

Involve epidermis, dermis, and underlying subcutaneous tissue
Appear white, cherry red. or black, with deep blisters; painless areas
Wound has dry, hard, leathery texture.
Treatment: often requires skin grafting

Answer 343

A

Fourth-Degree: Full-Thickness with Deeper Structures

Full-thickness injuries that extend beyond the dermis to involve muscle, bone, or both
Often occur in victims of high-voltage electrical injury or those with prolonged exposure to intense heat

Answer 344

A

Injuries to skin and soft tissue from unrelieved pressure
Tissue hypoxia occurs
Injury starts in deeper tissue before evident on the surface
Moisture and shearing add damage
Present over bony prominences

Answer 345

A

Stage 1 – nonblanchable erythema
Stage 2 – erythematous partial thickness loss of dermis; skin intact or ruptured blister
Stage 3 – full thickness skin loss with ulceration and adipose tissue visible
Stage 4 – full thickness skin loss with ulceration and visible fascia or deeper tissue; eschar present

Answer 346

A

Inflammatory skin disorder of the hair follicle and sebaceous gland
More common in adolescents and young adults
Four factors – hyperkeratinization; increased sebum; follicle bacteria; inflammation
Pathogenesis – increased androgen production increases sebum and keratinization blocks the hair follicle
Closed comedones – whiteheads
Open comedones – blackheads
Develop into papules, pustules, cysts
Occur more on face, neck and shoulders

Answer 347

A

Chronic inflammatory skin condition
More common in fair skinned and women
Abnormal skin response causing vasoactive and inflammatory manifestations
Typically affects the face – cheeks and nasal bridge
Erythematous spiderlike vessels, papules, pustules
Rhinophyma – more in men
Triggers – sun, sweating, stress, alcohol

Answer 348

A

Basal cell carcinoma – most common
Abnormal cell growth in lowest epidermis layer
Dry macular area; pearly nodule

Low metastatic potential

Answer 349

A

Squamous cell carcinoma
Changes in squamous cells in the middle epidermis layer – rapid growth
Smooth nodule or hyperkeratotic lesion
Can metastasize

Answer 350

A

Melanoma
Develops in the melanocytes
Can be life threatening

Answer 351

A

Asymmetry
Border – irregular
Color – tan, brown, black
Diameter – larger than 6 mm (pencil eraser)
Evolution – changing in size, shape, or color
Nonhealing or bleeding lesion

Answer 352

A

Growth issues, inflammatory hair follicle damage, or abnormalities in hair shaft
Scarring and nonscarring types
Alopecia areata
•Focal patches of hair loss; can be total loss

•Telogen effluvium

•Diffuse hair loss distribution

Patterned hair loss – male or female

Answer 353

A

•Onychomycosis – fungal nail

•Paronychia - staph bacterial cuticle infection

•Squamous cell CA and melanoma can present under the nail

•ABCDEF mnemonic for nail changes

Answer 354

A

Scleroderma

Collagen disease of unknown cause; fibrosis accompanied by inflammatory reactions and vascular changes in capillaries
Localized to the skin (benign) or produce systemic involvement (diffuse)
Localized: single or multiple, violet colored, firm, inelastic macules and plaques that enlarge slowly
Diffuse: skin hardens like hide, esophagus and gastrointestinal tract semi-rigid, lungs and heart fibrosis, and overlying tissue calcify; fatal

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