Last Test GI, Neuro, Skin Flashcards

Question

Acute Gastritis Patho and Clinical Manifestations

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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.

Answer 20

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

Answer 21

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

Answer 22

Hemolysis, ineffective erythropoiesis, resorption of large hematomas

Answer 23

Dysfunction of liver cells: increased levels of unconjugated bilirubin

Answer 24

Mechanical obstruction in bile duct causes conjugated hyperbilirubinemia

Answer 25

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

Answer 26

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

Answer 27

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\*\*\*

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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 39

+ 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

Answer 40

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 41

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 42

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 43

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 44

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 45

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 46

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

Answer 47

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 48

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 49

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

Answer 50

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 51

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 52

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 53

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

Answer 54

* Variceal bleeding * 30% will have hemorrhage within 2 years * Mortality 50% The greatest risk of rebleed occurs in first 72 hours

Answer 55

Causes: * Cholelithiasis - #1 cause * Alcohol abuse * Biliary dysfunction * Hypertriglyceridemia = \>600 * Pancreatic tumor

Answer 56

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 57

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 58

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 59

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 60

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 61

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 62

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 63

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 64

decreased fluid intake or excessing absorption slow motility medications decreased fiber diet spinal cord injury

Answer 65

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

Answer 66

* Inflammation of the vermiform appendix * Occurs as a result of obstruction

Answer 67

Inflammation of the peritoneum Pathogenesis * Chemical irritation – rupture GB or spleen * Direct organism invasion – appendicitis, abscess

Answer 68

Classic manifestation * Abdominal rigidity * Rebound tenderness * Nausea and vomiting * Fever, Leukocytosis

Answer 69

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 70

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

Answer 71

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

Answer 72

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 73

* 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 74

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 75

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 76

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 77

Ascending Colon

Answer 78

Last section of the small bowel

Answer 79

**_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 80

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 81

Clinical Manifestations: * Hematochezia * Melena * Loose stools/diarrhea * Abdominal cramping * Fluid and electrolyte imbalances * Anemia * Weight loss

Answer 82

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

Answer 83

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 84

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

Answer 85

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 86

Acute Diverticulitis - no colonoscopy Bowel perforation Peritonitis

Answer 87

Zankurs ## Footnote * Asymptomatic unless large * Gurgling in the throat, dysphagia * Risk for aspiration

Answer 88

Meckles ## Footnote * Mostly asymptomatic * Risk for ulceration and bleeding due to retained acid in the diverticulum

Answer 89

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 90

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 91

Adenocarcinoma Risk * Preserved and smoked foods * H. Pylori untreated * Smoking and alcohol * Genetics Pathogenesis * Localized tissue inflammation advances to dysplastic cells

Answer 92

* 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 93

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 94

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 95

* 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 96

* 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 97

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

Answer 98

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 99

* 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 100

•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 101

Clinical manifestations * Centrilobular emphysema * Pancreatic insufficiency * Cirrhosis symptoms

Answer 102

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

Answer 103

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

Answer 104

* 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 105

•Two major tracts 1. **_Dorsal column_**–medial lemniscal tract: fine touch, vibration, and proprioception• 2. **_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 106

•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 107

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

Answer 108

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 109

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 110

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 111

A Neural Tube defect where vertebrae does not fuse allowing the meninges and spinal cord herniation Related to Folate Deficiency in pregnancy

Answer 112

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 113

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 114

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 115

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

Answer 116

Meninges - Meningitis Brain parenchyma - Encephalitis

Answer 117

* 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 118

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

Answer 119

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 120

Brudzinski’s sign Flex neck with chin to the sternum and the hips flex more than they were

Answer 121

Kernig’s sign Flex knee and hip at 90 degrees and straightening the knee will cause lumbar pain

Answer 122

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 123

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

Answer 124

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 125

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 126

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 127

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

Answer 128

•Eyes, Verbal response, Motor response Mild – 13-15; Moderate 9-12; Severe \<8

Answer 129

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 130

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

Answer 131

* 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 132

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

Answer 133

* 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 134

Collection of blood between the dura and skull Rapid onset b/c it involves arteries Significant deterioration of consciousness usually involves skull fracture

Answer 135

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 136

* 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 137

Bleeding into the brain tissue Caused from HTN or contusions HA, Vomiting, Seizure, Unilateral Weakness

Answer 138

Quadriplegic

Answer 139

Paraplegia

Answer 140

Interruption of cerebral blood supply leading to necrosis of specified area of brain tissue Ischemic or hemorrhagic types

Answer 141

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 142

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

Answer 143

Associated with atherosclerosis and coagulopathies

Answer 144

Associated with cardiac dysfunction or dysrhythmias (atrial fibrillation)

Answer 145

Small penetrating infarcts need MRI to diagnose

Answer 146

* 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 147

•Neurologic symptoms typically last only minutes, but they may last as long as 24 hours. Symptoms resolve completely without evidence of neurologic dysfunction

Answer 148

* 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 149

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 150

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

Answer 151

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 152

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 153

* 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 154

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 155

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 156

Seizure and neurologic dysfunction due to hemorrhage

Answer 157

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 158

•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 159

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 160

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 161

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 162

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 163

•Provoked – brain trauma, hematomas, hypoglycemia, infection, chemicals Unprovoked - epilepsy

Answer 164

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

Answer 165

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

Answer 166

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 167

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 168

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

Answer 169

•Female; Vitamin D deficiency; EBV

Answer 170

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 171

Progressing-Relapsing MS Second Progressive MS Primary-Progressive MS Relapsing-Remitting MS

Answer 172

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 173

•Incidence * More males than females * Average age – 65 * Diagnosis to death – 15 years •Risk Factors: * Head trauma * Environmental toxins * Family history

Answer 174

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 175

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

Answer 176

Parkinson Stooped Posture Progression

Answer 177

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

Answer 178

•Clinical Manifestations * **Action Tremor** - worsens with activity * No rigidity of extremities * Usually bilateral * **Macrographia**

Answer 179

Pathogenesis: * Acute idiopathic paralysis of the CN VII facial nerve - unilateral Etiology: * Inflammatory; Compression; Viral (Herpes Simplex)

Answer 180

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 181

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 182

•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 183

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 184

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 185

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 186

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

Answer 187

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 188

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

Answer 189

Clinical Manifestations •Progressive dementia * Early impairment of attention, executive and visuospatial functioning, cognitive fluctuations * Daytime somnolence * Visual hallucinations * Parkinson features

Answer 190

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 191

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

Answer 192

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 193

Major depressive disorder (MDD) (5 symptoms) 1. Sad, empty, hopeless, loss of interest 2. Changes in weight, sleep, and activity 3. Fatigue 4. Diminished ability to concentrate or indecisiveness 5. Impaired functioning

Answer 194

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 195

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

Answer 196

Mania for at least one week alternating with episodes of MDD

Answer 197

Hypomanic episode of 4 day duration alternating with MDD symptoms

Answer 198

4 or more episodes of alternating moods in a year

Answer 199

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 200

Panic disorder – unexpected abrupt intense fear (perpetual) * Palpitations, diaphoresis, chest pain, dizziness

Answer 201

Generalized anxiety disorder – excessive worrying about life events * Present most days; less than 6 months * Restless, insomnia, fatigue

Answer 202

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 203

Bone to Bone

Answer 204

Muscle to bone

Answer 205

* 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 206

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 207

* Pathogenesis * Rare connective tissue disorder resulting in fragile bones and fractures Autosomal dominant disorder with mutation of collagen genes causing lax ligaments

Answer 208

Clinical manifestations Excessive and atypical fractures (child abuse suspected) May have short stature and limbs Hearing loss Premature osteoporosis

Answer 209

•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 210

•Lordosis – exaggerated concave lumbar spine * Develops in adolescent with poor posture; worsens with pregnancy and obesity; low back pain

Answer 211

•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 212

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

Answer 213

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

Answer 214

•Depressed fracture: fragment displaced below the level of the bone surface Face or Skull is common

Answer 215

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 216

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

Answer 217

•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 218

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 219

Clinical Manifestation * •Pain in joint or tenderness * •Swelling * •Erythema and warmth * •Fever if systemic Diagnosis CBC, ESR and CRP

Answer 220

* 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 221

_•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 222

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

Answer 223

•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 224

•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 225

* Clinical manifestations * Pain, stiffness, difficulty moving affected muscle, edema BRUISING Diagnosis with MRI and US

Answer 226

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

Answer 227

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

Answer 228

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 229

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 230

* 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 231

•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 232

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

Answer 233

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 234

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 235

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 236

Phalen Test for Carpal Tunnel Syndrome

Answer 237

•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 238

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

Answer 239

•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 240

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 241

•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 242

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

Answer 243

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

Answer 244

•Radiculopathy – damage near the nerve root at the spine

Answer 245

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

Answer 246

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

Answer 247

•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 248

•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 249

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 250

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

Answer 251

•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 252

•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 253

•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 254

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

Answer 255

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

Answer 256

•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 257

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 258

•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 259

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

Answer 260

* 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 261

•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 262

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 263

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 264

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 265

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 266

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 267

•Risk Factors * Males more than females * Obesity * Alcohol * Medications – thiazide and loop diuretics

Answer 268

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

Answer 269

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 270

Clinical manifestations Five characteristics 1. \<40 years old 2. Insidious onset 3. Improves with exercise 4. No improvement with rest 5. Pain worst at night and better with rising KYPHOSIS AND LOSS OF LUMBAR LORDOSIS (BACK FUSES STRAIGHT)

Answer 271

Pathogenesis Inherited, non-inflammatory disorders characterized by skeletal muscle degeneration Nine different forms Duchenne MD – most severe, most common affecting only males

Answer 272

* Clinical manifestations * Intellectual disability, muscle weakness, muscle spasms, poor coordination, delayed motor skills DIAGNOSE WITH MUSCLE BIOPSY

Answer 273

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 274

* 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 275

* ANA Qualitative screen - + or – * ANA Quantitative - ratio result 1:40 or greater is positive •ANA with reflex : Anti-SM Anti -dsDNA

Answer 276

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

Answer 277

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

Answer 278

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 279

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 280

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 281

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 282

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 283

Keratinocytes

Answer 284

Melanocytes

Answer 285

adipose cells

Answer 286

blood vessels

Answer 287

fibroblasts

Answer 288

* 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 289

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 290

* 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 291

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 292

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 293

•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 294

* 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 295

* 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 296

* 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 297

**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 298

•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 299

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

Answer 300

•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 301

•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 302

* 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 303

* Warts: common benign papillomas caused by DNA-containing papillomaviruses * Exaggeration of normal skin composition; s**tratum 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 304

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

Answer 305

•**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 306

•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 307

* 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 308

* 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 309

* 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 310

* 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 311

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 312

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 313

•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 314

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

Answer 315

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 316

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 317

Second-Degree: Deep Partial-Thickness Burns ## Footnote * **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 318

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: o**ften requires skin grafting**

Answer 319

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 320

* 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 321

* 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 322

* 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 323

* 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 324

* Basal cell carcinoma – **most common** * Abnormal cell growth in **lowest** epidermis layer * Dry macular area; pearly nodule **Low metastatic potentia**l

Answer 325

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

Answer 326

* Melanoma * Develops in the melanocytes * Can be life threatening

Answer 327

* 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 328

* 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 329

**•Onychomycosis** – fungal nail •**Paronychia** - staph bacterial cuticle infection _•Squamous cell CA and melanoma can present under the nail_ •ABCDEF mnemonic for nail changes

Answer 330

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