UW NEURO

Question 1

Broca

Answer 1

Sparse & non fluent speech
Comprehension preserved
Repetition impaired
Right hemiparesis (face&upper limb)

Question 2

Wernicke

Answer 2

Fluent and voluminous but lacks meaning
Comprehension diminished
Repetition impaired
Right Sup visual field defect

Question 3

How does Broca lead to ipsilateral motor issues

Answer 3

The lesion often extends beyond Broca, extending into the ipsilateral motor regions

Question 4

Phrenic nerve

Answer 4

C3-C5 nerve roots deliver motor innervation to the diaphragm and carries pain fibers from the diaphragmatic and mediastinal pleura

Question 5

Differences btwn the location where the gracile and cuneate fasiculi appear

Answer 5

Gracile and cuneate fasiculi are present above the T7 spinal level where as gracile fasciculus is present below this level

-so the cuneate fasiculus doesn’t appear until above T7 spinal level

Question 6

Describe spinal cord changes as you move rostrally

Answer 6

As you move rostrally, spinal level increase the amount of white matter, dec amount of grey mater and are more oval shaped

Question 7

What are features that the spinal cord has at the thoracic and lumbar section that others don’t?

Answer 7

Contain lateral gray horns (intermediate cell columns)

Question 8

What pathway is the medial geniculate bodies a part of ?

Answer 8

Auditory pathway along with the inferior colliculi

Question 9

Where does the right lateral geniculate receive visual information from?

Answer 9

Right temporal he ire Tina and left nasal hemiretina

Question 10

Innervation of the gluteus maximus

Answer 10

Inferior and superior gluteal nerve

Question 11

Superior gluteal nerve injury

Answer 11

Results in weakness and paralysis of the gluteus medius, gluteus minimus, tensor fascinate latae muscles–>trendelenburg sign

Question 12

External Iliac

Answer 12

Supplies the inferior epigastric artery and deep circumflex Iliac artery before becoming the femoral artery

Question 13

Common results of degenerative arthritis of the spine (narrowing in the spinal canal due to Inter vertebral disk herniation

Answer 13

Ligemtum flavin hypertrophy, osteophyte formation affecting the facet joints

Question 14

Meningiomas

Answer 14

Adult intracranial tumors that arise in the rural reflections (falx cerebri, tentorium cerebelli)
Look at where the lesion is occurring:
-if in the primary somatosensory cortex: contralateral sensory loss
-damage to the parietal association cortex (in the non-dominant hemisphere) causes impaired visual spatial processing

Question 15

Annular Pancreas

Answer 15

Pancreatic tissue encircling the descending duodenum caused by abnormal migration of the ventral pancreatic bud

Question 16

Acute Cholecystitis

• cause?
• signs to ID?

Answer 16

Caused by gallstone obstructing the cystic duct

• finding signs of gall bladder inflammation (wall thickening, pericholecystic fluid) on ultrasonography
• if inconclusive then nuclear medicine scan to access the cystic duct Patency and make the diagnosis.

Question 17

Primary Biliary cirrhosis

Answer 17

Autoimmune destruction of intrahepatic bile ducts and cholestasis (inc Alk Phosphatase)

Question 18

PBC clinical presentation

Answer 18

Pruritus, fatigue, hepatosplenomegaly, xanthomatous lesions in the eyelids, skin or tendons

Question 19

Which Syndrome arises secondary to thrombotic occlusion of the hepatic veins and/or suprahepatic Inferior Vena Cava

Answer 19

Budd-Chiari

-venous occlusion causes inc sinusoidal pressure to increase leading to inc portal HTN, ascites, hepatomegaly, splenomegaly

Question 20

Which diagnostic marker is present in Primary Biliary Cirrhosis

Answer 20

Anti-mitochondrial Antibody

Question 21

Lac Operon regulation

Answer 21

-negatively by binding of the repressor protein to the operator locus
-positively by cAMP-CAP binding upstream from the promoter region
Glucose decreases the activity of adenylyl cyclase (reducing intracellular cAMP), the lac operon is repressed in high glucose conditions

Question 22

Rifaximin

Answer 22

Used in patients with hepatic encephalopathy

-metabolized by intestinal bacteria to short Chain fatty acids, lowering the pH = more conversion of ammonia to ammonium

Question 23

Treatments for hepatic encephalopathy

Answer 23

Lactulose (inc conversion of ammonia to ammonium) and rifaximin ( dec intraluminal ammonia production)

Question 24

Scleroderma esophagus effect

Answer 24

Impaired motility
-incompetent LES
Gastroesophageal reflux

Question 25

Achalasia manometry

Answer 25

Decreased peristalsis in the mid esophagus, with increased tone and incomplete relaxation at the LES -reduced inhibitory neurons in the esophageal wall-->imbalance favoring excitatory ganglion cells

Question 26

NK cells

Answer 26

Kill cells with decreased MHC class I antigen cell surface expression such as virus infected cells and tumor cells

Question 27

Common causes of gastric ulcers

Answer 27

NSAIDS, surgical stress, head trauma (cushing ulcers), curling ulcers, smoking, alcohol consumption

Question 28

Erosions vs ulcers

Answer 28

Erosions: mucosal defects that do not fully extend through the muscular is mucosa

Question 29

Granulomatous destruction of bile ducts

Answer 29

Primary Biliary cirrhosis

Question 30

Hepatocellular accumulation of coarse pigmented granules making liver appear black

Answer 30

Dubin Johnson syndrome: autosomal recessive disorder causing conjugated hyperbilirubinemia

Question 31

Clinical presentation of Biliary Atresia

Answer 31

Obstruction of extra hepatic ducts--> presents with jaundice, dark urine, acholic stools = conjugated hyperbilirubinemia

Question 32

Gilbert syndrome

Answer 32

Reduced production of glucorynyl transferase ( dec glucurodination) -patients are usually asymptomatic except at times of stress ( fasting,illness) during which mild hyperbilirubinemia and jaundice are present

Question 33

Does secretory diarrhea improve with dietary modification?

Answer 33

No

Question 34

What would be a clinical presentation of a VIPoma

Answer 34

Watery diarrhea (inc Cl secretions), hypokalemia, achlorhydria Also inc cAMP causing sodium, cl, water secretin in the bowel

Question 35

Mallory Weiss tear clinical presentation

Answer 35

Vomiting, retching, hematemesis, epigastric pain

Question 36

Linear tear near the gastroesophageal junction Caused by forceful vomiting Submucosal or venous plexus bleeding

Answer 36

Mallory weiss tear | -the repetitive vomiting can leas to metabolic alkalosis

Question 37

Clinical presentation of Boerhaave syndrome

Answer 37

Vomiting, retching, Chest and upper abdominal pain, Fever, dyspnea, septic shock

Question 38

Hep D and B connection

Answer 38

HDAg is considered replication defective bc it must be coated by Hep B ext coat HBAsg to penetrate hepatocyte

Question 39

Tropheryma Whippelii stain

Answer 39

PAS -->magenta stain highlighting polysaccharides of the fungal cell wall

Question 40

Fibrates connection to gallstones

Answer 40

Inhibit the enzyme cholesterol 7 alpha hydroxylase that converts cholesterol to bile -so you get less cholesterol being converted to bile

Question 41

Gall bladder sludge formation

Answer 41

Precursor to stone formation | Gall bladder function to concentrate bile by actively absorbing water from the bile

Question 42

Pigment gallstones

Answer 42

Brown or black and arise from conditions that increase the amount of unconjugated bilirubin in bile

Question 43

Pancreatic Divisum

Answer 43

Ventral and dorsal pancreatic buds fail to fuse | Pancreatic secretions out via separate ducts

Question 44

Chrons and oxalate kidney stones

Answer 44

Impaired bile acid absorption in the terminal ileum leads to loss of bile acids in feces so inc fat. The inc lipids bind calcium =more free oxalate that precipitates, absorbed forming urinary calculus -normally the oxalate would bind to calcium forming an unabsorbable complex

Question 45

Transmural esophageal tear caused by forceful vomiting | -esophageal air/fluid leakage into the mediastinum and pleura

Answer 45

Boerhaave syndrome