UW NEURO Flashcards

1
Q

Broca

A

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

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2
Q

Wernicke

A

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

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3
Q

How does Broca lead to ipsilateral motor issues

A

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

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4
Q

Phrenic nerve

A

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

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5
Q

Differences btwn the location where the gracile and cuneate fasiculi appear

A

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

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6
Q

Describe spinal cord changes as you move rostrally

A

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

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7
Q

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

A

Contain lateral gray horns (intermediate cell columns)

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8
Q

What pathway is the medial geniculate bodies a part of ?

A

Auditory pathway along with the inferior colliculi

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9
Q

Where does the right lateral geniculate receive visual information from?

A

Right temporal he ire Tina and left nasal hemiretina

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10
Q

Innervation of the gluteus maximus

A

Inferior and superior gluteal nerve

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11
Q

Superior gluteal nerve injury

A

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

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12
Q

External Iliac

A

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

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13
Q

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

A

Ligemtum flavin hypertrophy, osteophyte formation affecting the facet joints

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14
Q

Meningiomas

A

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

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15
Q

Annular Pancreas

A

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

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16
Q

Acute Cholecystitis

  • cause?
  • signs to ID?
A

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.
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17
Q

Primary Biliary cirrhosis

A

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

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18
Q

PBC clinical presentation

A

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

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19
Q

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

A

Budd-Chiari

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

20
Q

Which diagnostic marker is present in Primary Biliary Cirrhosis

A

Anti-mitochondrial Antibody

21
Q

Lac Operon regulation

A

-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

22
Q

Rifaximin

A

Used in patients with hepatic encephalopathy

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

23
Q

Treatments for hepatic encephalopathy

A

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

24
Q

Scleroderma esophagus effect

A

Impaired motility
-incompetent LES
Gastroesophageal reflux

25
Q

Achalasia manometry

A

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

26
Q

NK cells

A

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

27
Q

Common causes of gastric ulcers

A

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

28
Q

Erosions vs ulcers

A

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

29
Q

Granulomatous destruction of bile ducts

A

Primary Biliary cirrhosis

30
Q

Hepatocellular accumulation of coarse pigmented granules making liver appear black

A

Dubin Johnson syndrome: autosomal recessive disorder causing conjugated hyperbilirubinemia

31
Q

Clinical presentation of Biliary Atresia

A

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

32
Q

Gilbert syndrome

A

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

33
Q

Does secretory diarrhea improve with dietary modification?

A

No

34
Q

What would be a clinical presentation of a VIPoma

A

Watery diarrhea (inc Cl secretions), hypokalemia, achlorhydria

Also inc cAMP causing sodium, cl, water secretin in the bowel

35
Q

Mallory Weiss tear clinical presentation

A

Vomiting, retching, hematemesis, epigastric pain

36
Q

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

A

Mallory weiss tear

-the repetitive vomiting can leas to metabolic alkalosis

37
Q

Clinical presentation of Boerhaave syndrome

A

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

38
Q

Hep D and B connection

A

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

39
Q

Tropheryma Whippelii stain

A

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

40
Q

Fibrates connection to gallstones

A

Inhibit the enzyme cholesterol 7 alpha hydroxylase that converts cholesterol to bile

-so you get less cholesterol being converted to bile

41
Q

Gall bladder sludge formation

A

Precursor to stone formation

Gall bladder function to concentrate bile by actively absorbing water from the bile

42
Q

Pigment gallstones

A

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

43
Q

Pancreatic Divisum

A

Ventral and dorsal pancreatic buds fail to fuse

Pancreatic secretions out via separate ducts

44
Q

Chrons and oxalate kidney stones

A

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

45
Q

Transmural esophageal tear caused by forceful vomiting

-esophageal air/fluid leakage into the mediastinum and pleura

A

Boerhaave syndrome