Classic Presentations Flashcards

Clinical Presentation on the Question side, and Diagnosis / Disease on the other side

1
Q

Abdominal pain
Ascites
Hepatomegaly

A

Budd Chiari Syndrome (aka Post-Hepatic Venous Thrombosis)

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2
Q

Achilles Tendone Xanthoma

A

Familial Hypercholesterolemia (Decrease LDL Signaling)

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3
Q

Adrenal Hemorrhage
Hypotension
DIC

What is the pathogen that leads to this presentation?

A

Waterhouse - Friedrichson Syndrome (Meningococcemia)

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4
Q

Arachnodactlyly
Lens Dislocation
Aortic Dissection
Hyperfelxible joints

A

Marfan’s Syndrome

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5
Q

A mutation in which gene leads to Marfan’s Syndrome?

A

Fibrillin gene

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6
Q

Athlete with polycythemia

A

Secondary to EPO injection

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7
Q

Back pain
Fever
Night sweats
Weight Loss

A

Pott’s Disease

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8
Q

Pott’s Disease is caused by_____?

A

Vertebral TB

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9
Q

Bilarteral Hilar Adenopathy

Uveitis

A

Sarcoidosis

non-caseating granulomas

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10
Q

Blue Sclera

A

Osteogenesis Imperfecta

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11
Q

Bluish linie on gingiva

A

Burton’s line

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12
Q

Burton’s line is caused by____?

A

Lead Poisoning

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13
Q

Bone Pain
Bone Enlargement
Arthritis

A

Paget’s Disease of Bone

increase of osteoblastic and osteoclastic activity

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14
Q

Bounding Pulses
Diastolic Heart Murmur
Head Bobbing

A

Aortic Regurgitation

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15
Q

“Butterfly” facial rash

Raynaud’s phenomenon in a young female

A

SLE

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16
Q

Cafe-au-lait spots
Lish Nodules
Iris Hamartoma

(+pheochromocytoma, Optic Gliomas)

A

Neurofibomatosis Type I

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17
Q

Cafe-au-lait spots
Polyostotic fibrous dysplasia
Precocious Puberty
Multiple Endocrine Abnormalities

A

McCune Albright Syndrome

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18
Q

Which Mutation causes McCune Albright Syndrome?

A

Mosaic G-Protein Signaling mutation

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19
Q

Calf pseudohypertrophy

A

Muscular dystrophy

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20
Q

What movement is characteristic of Muscular Dystrophy?

A

Gower’s Maneuver

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21
Q

What mutation causes Muscular dystrophy?

A

X-linked Recessive mutation of dystrophin gene

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22
Q

“Cherry - Red Spot” on Macula

Individual causes

A

Tay-Sachs: Ganglioside accumulation

Neimann-Pick Disease: Sphingomyelin accumulation

Central Retinal Artery Occlusion

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23
Q

chest pain on exertion

A

Angina:

Stable - with moderate exercise

Unstable - with minimal exercise

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24
Q

Chest pain
pericardial effusion/ friction rub
Persistent fever following MI

A

Dressler’s Syndrome

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25
Q

What is the cause of Dressler’s Syndrome?

A

Auto-immune mediated Post-MI fibrinous pericarditis

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26
Q

When is it common to see Dressler’s syndrome post an MI?

A

1-12 weeks

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27
Q

Child uses arms to stand up from squat

A

Gower’s Maneuver

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28
Q

Child with fever later develops red rash on face that spreads to body

A

“slapped cheeks”

Erythema infectious/ 5th Disease: parvovirus B19)

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29
Q

Chorea
Dementia
caudate degeneration

What causes this?

A

Huntington’s Disease

ADDx: CAG repeat expansion
MC: 30-40 years
shows anticipation

insidious onset of personality and then physical changes:

personality: Aggressiveness, Flat affect, depression, or anxiety, dec. memory, concentration, psychosis.

Movement:
purposeless movement, choreiform movements, bradykinesia

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30
Q

Chronic exercise intolerance with myalgia
Fatigue
Painful cramps
myoglobinuria

A

McArdle’s Disease

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31
Q

What causes McArdle’s Disease?

A

Muscle Glycogen Phosphorylase Deficiency

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32
Q

Cold Intolerance

A

Hypothyroidism

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33
Q

Heat Intolerance

A

Hyperthyroidism

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34
Q

Conjugate lateral gaze palsy

Horizontal diplopia

A

Internuclear ophthalmoplegia (damage to MLF)

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35
Q

Bilateral INO

A

Multiple Sclerosis

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36
Q

Unilateral INO

A

Stroke

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37
Q

Continuous “machinery” heart murmur

A

PDA

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38
Q

How do you close a PDA? Keep it open/maintain?

A

Close: Indomethicin
Open: Misoprostol

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39
Q

Cutaneous/ Dermal edema due to connective tissue deposition

A

Myxedema

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40
Q

Cause of Pre-tibial Myxedema?

A

Hypothyroidism

Grave’s Disease

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41
Q

Dark Purple skin

Mouth Nodules

A

Kaposi’s Sarcoma
Usually seen in AIDS patients
Associated with HHV-8

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42
Q

Deep, Labored Breathing

Hyperventilation

A

Kussmaul breathing

associated with DKA

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43
Q

Dermatitis
Dementia
Diarrhea

A

Pellagra

B3-Df

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44
Q

Dilated Cardiomyopathy
Edema
Alcoholism or malnutrition

A

Wet Beri-Beri (Vitamin B1 Df.)

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45
Q

Dog or cat bite resulting in infection

How does this present?

A

Pasteurella multocida

Presents as cellulitis at inoculation site

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46
Q

Dry eyes
Dry Mouth
Arthritis

A

Sjogren’s syndrome

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47
Q

What causes Sjogren’s Syndrome

A

Autoimmune destruction of exocrine glands

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48
Q

Dysphagia (esophageal webs)
Glossitis
Iron Deficiency Anemia

A

Plummer-Vinson Syndrome (may progress to esophageal squamous cell carcinoma)

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49
Q

Elastic Skin, hyper mobility of joints

A

Ehlers-Danlos Syndrome

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50
Q

Erythroderma
Lympadenopathy
Hepatosplenomegaly
Atypical T Cells

A

Sezary Syndrome (Cutaneous T-Cell Lymphoma)

OR

Mycosis fungoides

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51
Q

Facial muscle spasm when tapped

A

Chvostek’s Sign

Indicative of Hypocalcemia

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52
Q

Fat
Female
Forty
Fertile

A

Cholelithiasis

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53
Q

Fever
Chills
headache
myalgia following ABx treatment for syphilis

A

Jarisch-Herxheimer Rxn

rapid lysis of spirochetes results in toxin release

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54
Q
Fever
Cough 
Conjunctivitis
Coryza
Diffuse Rash
A

Measles

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55
Q

Fever
Night sweats
Weight Loss

A

B-symptoms

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56
Q

Fibrous Plaques in soft tissue of penis

A

Peyronie’s Disease (CT Ds)

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57
Q

Gout
Mental Retardation
Self-mutilating Behavior in a boy

A

Lesch-Nyhan Syndrome

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58
Q

What causes Lesch-Nyhan Syndrome?

A

HGPRT Df. X-Linked Recessive

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59
Q

Green-yellow rings around peripheral cornea

A

Kayser-Fleiscer rings from Copper Accumulation in Wilson’s Syndrome

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60
Q

Hamartomatous GI Polyps

Hyperpigmentation of Mouth, Feet and Hands

A

Peutz-Jergers Syndrome

Inherited, benign polyposis can cause bowel obstruction

carries an increased cancer risk - Mainly GI

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61
Q

Hepatosplenomegaly
Osteoporosis
Neurologic Symptoms

A

Gaucher’s Disease

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62
Q

What causes Gaucher’s Disease

A

Glucocerebrosidase Df.

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63
Q

Hereditary nephritis
Sensorineural Hearing loss
Cataracts

A

Alports Syndrome (mutation in the Type IV collagen in GBM)

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64
Q

Hyperphagia
Hypersexuality
Hyperorality
Hyperdocility

A

Kluver Bucy Syndrome

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65
Q

What causes Kluver-Bucy Syndrome

A

Bilateral Amygdala lesion

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66
Q

Hyperrefelxia
Hypertonia
Babinki signt present

A

UMN lesion

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67
Q

Hyporeflexia
hypotonia
Atrophy
Fasciculations

A

LMN lesion

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68
Q

Hypoxemia
Polycythemia
Hypercapnia

A

“Blue Bloater” COPD = Chronic Bronchitis due to hyperplasia of the mucous cells

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69
Q

Indurated, ulcerated genital lesion

A

Non-painful: chancre (Primary Syphilis, Preponema pallidum

Painful, with exudate: chancroid (Haemophilus ducreiyi)

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70
Q
Infant with cleft lip/palate
microcephaly
holoprosencephaly
polydacyly
cutis aplasia
A

Patau’s Syndrome

Trisomy 13

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71
Q

Infant with failure to thrive
Hepatosplenomegaly
Neurodegeneration

A

Niemann - Pick Disease

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72
Q

What causes Niemann-Pick Disease?

A

genetic sphingomyelinase deficiency

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73
Q

Infant with hypoglycemia
Failure to thrive
Hepatomegaly

A

Cori’s Dx

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74
Q

What causes Cori’s Disease?

A

Debranching Enzyme Df.

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75
Q

Infant with microcephaly
Rocker-bottm feet
Clenched hands
Structural heart defect

A

Edward’s Syndrome (Trisomy 18)

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76
Q

Jaundice

Palpable distended non-tneder gallbladder

A

Couvoisier’s sign - distal obstruction of biliary tree

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77
Q

Large rash with bull’s eye appearance

A

Erythema chronic migraines from Ixodes tick bite

Lyme Dx: Borrelia

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78
Q

Lucid interval after TBI

A

Epidural hematoma

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79
Q

Most common artery that breaks in a Epidural Hematoma?

A

Middle Meningeal artery

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80
Q

Male child
Recurrent infections
No Mature B-Cells

A

Burton’s disease

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81
Q

What causes Burton’s disease?

A

X-Linked agammaglobulinemia

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82
Q

Mucosal bleeding and prolonged bleeding time

A

Glanzmann’s thrombasthenia (defect in PLT aggregation due to lack of GpIIb/IIIa)

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83
Q

Cause of Glanzmann’s thrombasthenia

A

defect in PLT aggregation due to lack of GpIIb/IIIa

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84
Q

Muffled heart sounds
distended neck veins
Hypotension

A

Beck’s triad of cardiac tamponade

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85
Q

Multiple colon polyps
Osteomas/ soft tissue tumors
impacted/supernumarary teeth

A

Gardner’s syndrome (subtype of FAP)

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86
Q

“Thyroidization” of the Kidneys: with which Disorder is it associated?

A

Chronic Pyelonephritis

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87
Q

recently hospitalized patient displays spastic quadriplegic…what could have happened and why?

A

Central Pontine Myelinolysis: Destroys the corticospinal tracts creating a “locked in Syndrome”

Note: Locked in Syndrome can also be caused by an occlusion of the basilar artery

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88
Q

Triad: dysarthria, dysphagia, and head/neck muscle weakness that presents in addition to quadriplegia

A
The other half of Central Pontine Myelinolysis: Pseudobulbar palsy. 
Demyelination of:
CN IX: can't talk
CN X: can't swallow
CN XI: head and neck muscle weakness

This is called pseudo bulbar because it is a DEMYELINATING disorder, which by definition means that you are affecting the axons. Bulbar palsy however, is caused by degeneration of the associated nuclei of the CN listed above.

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89
Q

Rapid correction of Hypernatremia leads to

A

Cerebral edema

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90
Q

Rapid correction of Hyponatremia

A

Central pontine myelinolysis

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91
Q

Capropedal spasm

A

Spasmodic movement of the hands +/- feet

Caused by Hypocalcemia

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92
Q

Chvostek’s sign

A

twitching if the jaw by tapping the mandibular nerve.

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93
Q

Early onset ataxia with repeated sinopulmonary infections, and then abnormal dilatations of the capillary vessels of the eye.

A

ARDx: Faulty DNA Repair after Ionizing radiation

Ataxia-Telangiectasia

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94
Q

Chromosomal Instability Ds

A
  1. Ataxia-Telangiectasia: Unable to repaire non-homologous end-joining caused by Ionizing radiation
  2. Xeroderma Pigmentosa: NER: UV Light (premature skin aging and increased risk of skin cancer = malignant melanoma and SCC)
  3. Fanconi syndrome: HS of DNA to cross-linking agents
  4. Bloom Syndrome: Generalized chromosomal instability - increased susceptibility to neoplasms
  5. HNPCC: defect in MMR
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95
Q

Neurofibrillary tangles

A

Alzheimer’s Dx

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96
Q

Loss of neurons in the substantial nigra pars compacta

A

PDx

Presents with memory impairment, cogwheel rigidity, bradykinesia, masked facies. The dementia is gradual

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97
Q

Bilateral Atrophy of the Caudate and putamen

A

Huntington’s

In addition: Caudate atrophy shows
dilation of the frontal horns of the lateral ventricles, and microscopy of the atrophic areas reveals gliosis and neuronal loss

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98
Q

Posterior DCML demyelination

A

B12 or syphilis

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99
Q

Lewy bodies

A

PDx OR

Lewy Body dementia

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100
Q

VMN

A

Nml: satiety
AB: hyperphagia
(+) letpin

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101
Q

LMN

A

Nml: hunger
AB: Anorexia
(-) leptin

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102
Q

AMN

A

N: heat dissipation via PSNS
A: hypothermia

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103
Q

PMN

A

N: Heat conservation via the SNS
A: hypothermia

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104
Q

Arcuate

A

Secretes DA to (-) PRL, GHRH, GnRH

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105
Q

PVNM

A

ADH, CRH, Oxytocin, TRH secretion

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106
Q

Supraoptic Nucleus

A

ADH and Oxytocin secretion

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107
Q

Suprachiasmatic Nucleus

A

Circadian rhythm and pineal gland function (melatonin)

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108
Q

Jet Lag represents disorder in what hypothalamic nucleus?

A

Suprachiasmatic nucleus

Dyssynchrony between the body’s circadian rhythms and the environment (i.e. light): insomnia, daytime sleepinesss, dec. work performance, GI issues, and malaise.

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109
Q

Input into the Suprachiasmatic nucleus comes from ___

A

Photosenstative ganglion in the retina = retina hypothalamic tract.

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110
Q

the suprachiasmatic regulates the circadian rhythm by modulating ___

A
modulates body temperature (inc. in morning)
cortisol levels (why its higher with no sleep)
melatonin levels (induction of sleep). should be highest at night, lowest in the middle of the night
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111
Q

Traveling which direction takes a longer time to resynchronize the suprachiastmatic nucleus?

A

Eastward travel > Westward

its easier to lengthen the sleep/wake cycle than it is to shorten it.

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112
Q

sudden spike in prolactin that is drug induced

A

typically antipsychotics that have more D2>5HTx. these would be typical anti-psychotics

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113
Q

galactorrhea

A

regulated by increased prolactin. normal post-delivery, abnormal any other time

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114
Q

tuberoinfundibulnar dopaminergic pathway

A

connects the hypothalamus and the pituitary gland. DA (-) PRL release.

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115
Q

Sx of high prolactin (with no tumor)

A

galactorrhea
changes in menstrual cycle
Sexual dysfunction

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116
Q

Mesolimbic - mesocortical pathway

A

regulates behavior and is the most disrupted in Schizophrenia, where the tonic control of the Mesolimbic pathway over the mesocortical is missing

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117
Q

Nigrostriatal pathway

A

Substantia nigra to the caudate nucleus and the putamen (in this sentence both PDx and HDx is covered).
This pathway has DA (-) ACh release

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118
Q

Why can the Tx with high dose anti-psychotics present with parkinsonian features?

A

because they disrupt the DA (-) over ACh in the nigrostriatal pathway that controls movement (via basal ganglia)

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119
Q

What are the 3 important DA pathways?

A
  1. Tuberoinfundibular (DA (-) PRL release)
  2. Nigrostriatal (DA (-) ACh)
  3. Mesolimbic-Mesocortical (DA (-) 5HTx)
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120
Q

Necrosis due to ischemic injury presents with what two features? Which organ is the one exception to the rule?

A

Ischemia will almost always lead to Coagulative Necrosis. the one organ that is exempt is the brain, which presents with liquifactive necrosis.

  1. Presents with initial preservation of cytoarchictecture
  2. a nucleated eosinophillic cytoplasm
  3. eventual Leukocytes clean up the mess
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121
Q

Liquifactive necrosis is due to _____, and presents with what features?

A

Causes: focal bacterial infections that (+) WBC reaction
Predominant form of necrosis in the brain
1. Necrotic cells are digested, no cytoarchitecture preserved
2. viscous liquid mass made
3. necrotic fluid becomes filled with pus, and is assoc. with abscess formation in the peripheral tissues. In the brain it will be CSF-filled spaces.

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122
Q

Fat Necrosis

A

Seen with acute pancreatitis - enzymatic activation will self-digest.
Seen with saponification (chalky -white deposits that form with FFA)

Note: this is also seen in the gut. it is not recommended to take calcium with fatty foods - will not absorb.

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123
Q

Caseous necrosis

A
TB infection (MC)
Histoplasma
Cryptococcus
Coccidioses
Cheesy tan-white gross appearance
Consits of fragmented cells 
surrounded by M0 =  granuloma
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124
Q

Left MCA stroke

A

R. hemiparesis

Dysphagia

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125
Q

the brain will present with full on liquifactive necrosis in __ Days

A

10

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126
Q

Fibrinoid necrosis

A

Histologic pattern of injury seen in the vessel walls that are affected by:
Vasculits (i.e. PAN)
Malignant HTN
DM

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127
Q

Non-enzymatic Fat necrosis occurs due to

A

trauma
MC is the female breast
often mistaken for a tumor

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128
Q

Broca’s Aphasia

A
"Broca = Broken Speech"
Broadman Area 44/45
Communication motor planning
Patient will be able to talk but they have to think about how to make every word. Comprehension is intact, and they have a hard time repeating anything. 
Associated with r. hemiparesis
MCA stroke
typically a frustrated patient
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129
Q

Wernicke’s aphasia

A

Word Salad
Poor comprehension
rep. impaired
Associated with R. Superior visual Field defect

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130
Q

Damage to frontal eye field?

A

Located directly anterior to the pre-central gyrus

Damage = Ipsilateral deviation

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131
Q

Pre- central gyrus

A

Primary motor cortex

  • dysarthria
  • paresis/ paralysis
  • trouble moving mouth, tongue, and larynx.
  • hemiparesis
  • apraxia
  • NO language involved.
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132
Q

MCC aseptic meningtitis

A

Viral
Enteroviruses
coxsackievirus, echovirus, poliovirus, and enterovirus = 90% of cases

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133
Q

HA
Fever
Neck stiffness

A

Viral Meningitis
Spinal tap will differentiate the types.
+/- photophobia, lethargy

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134
Q

Focal Neurologic Signs
Stupor
Photophobia
Fever

A

Bacterial Meningitis

in only 40% of cases do you see nuchal rigidity

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135
Q

MCC Bacterial Meningitis

A

S. pneumonia
N. meningitidis

(in neonates = Listeria and GBS)

136
Q

meningitis + parotitis

A

seen in 50% of mumps cases

137
Q

MCC common cold

A

Coronavirus
Rhinovirus
Adenovirus (Also the MCC of monocular conjunctivitis)

138
Q

MCC of meningitis in AIDS patients

A

Cryptococcal Meningitis

DDx: India ink stain

139
Q

Acute onset difficulty walking with bilateral extremity weakness
Seen with absent DTRs
PMH reveals GI infection

A

c. jejuni - MCC of infectious diarrhea and it is the

MCC of GBS

140
Q

Demyelinating syndromes of the peripheral nerves

A

GBS

Ascending paralysis that can lead to respiratory failure

141
Q

diplopia
dysphagia
dysphonia

A

The 3 D’s of Botulinum Toxin

Occurs within 12-46 hrs of exposure

142
Q

types of botulism

A

Food-borne
Wound
infant (honey)

143
Q

confusion
HA
Inflammatory CSF

A

Meningitis

144
Q

C. neoformans

A
  • Narrow based buds with thick capsule
  • soil/pigeon droppings
  • Primary: Lung
  • MC: meningoencephalitis
  • Can disseminate
    DDx: India Ink + Latex agglutination (poly.capsule) of CSF
    Growth: Sabouraud’s agar
145
Q

Methenamine

A

Mucicarmine stains fo tissue = C. neoformans

146
Q

Tx of c. neoformans

A

Amphotericint B + Flucytosine (Acute)

Fluconazole (prophylaxis)

147
Q

Non-septate hyphae

A

Wide angle: Mucor/Rhizopus
- love DM/leukemia patients
Narrow angle: Aspergillus

148
Q

Germ tubes

A

C. albicans

to see germ tubes you have to incubate at 37 degrees for 3 hours

149
Q

spherules

A

Coccidiodes immitis
Lung Dx
Disseminated mycosis

150
Q

How many Ub indicate destruction tag?

A

4

151
Q

Parkin
PINK-1
DJ-1
mutations

A

ARDx form of PDx (<50y/o)

leads to a breakdown in the Ub-Proteosome system

152
Q

Histone acetylation promotes_____

A

euchromatin

153
Q

Histone deacetylation promotes

A

Heterochromatin

154
Q

Df. of bilirubin glucuronidase

A

Crigler-Najjar Syndrome

Complete Df is fatal

155
Q

Ophthalmoplegia
Ataxia
confusion

A
"Eyes, Lies, Capsize"
Wernicke Syndrome
lethal in 10-20%
due to B1 Df. 
commonly seen in the malnourished (classic patient is an alcoholic)

Will show foci of hemorrhage and necrosis in the MAMILLARY BODIES and PAG

Tx: B1 + Glc

156
Q

vitamin B1: Rxns

A

Pyruvate dehydrogenase
alpha-ketoglutarate dehydrogenase
Transketolase (PPP - pensose to G3P)

157
Q

Wernicke Syndrome: DDx

A

increase in RBC transketolase levels after B1 infusion

158
Q

G6PD Df

A

RLS in PPP: hemolytic anemia

159
Q

Methylmalonic acid

A

product of FFA oxidation

converted to succiyl-CoA by methylmalonyl-CoA mutase with the help of B12

160
Q

B12

A

Methylmalonyl-CoA mutase

DDx: increased methylmalonic acid, which will not be present in Folic acid df.

161
Q

why does a df. in B1 lead to Wernicke Syndrome?

A

the brain can’t utilize glucose as well because it is so critical to the Kreb’s Cycle and the FFA beta-Oxidation

162
Q

pale catecholaminergic nuclei
pale hair, skin
light eyes

A
PKU
can't use phenylalanine =  no DA, NE, E
No melatonin (Tyrosinase can't convert nothing)
163
Q

abdominal pain
neuropsychiatric changes
darkening of urine

A

acute intermittent porphyria

164
Q

Valproate in a pregnant woman

A

Teratogenic
Neural tube defect - meningocele
Why?
Valproate (-) intestinal Folic Acid uptake

165
Q

coarctation of aorta + bicuspid aortic valve = Most Likely Ds

A

Turner Syndrome

166
Q

Duodenal Atresia = associated congenital disorder

A

Downs

  • bilious vomiting w/o abominal distension
    Typically seen on 1st day of life
    Peristaltic wave may be appreciated
    Commonly (+) History of polyhydramnios
167
Q

Potter Sequence results in

A

Renal agenesis and Lung hypoplasia

typically spontaneously abort

168
Q

Lithium in pregnancy

A

Ebstein’s anomaly
“atrialized RV”
Downward displacement of tricuspid and thin IV septum

169
Q

Mature defenses

A

Suppression: intentional withholding of distressing unconscious material
Humor: making light of ___
Altruism: ameliorated feeling of guilt by giving to others without solicitation

170
Q

Immature defenses

A

Repression: trigger releases a stored memory
Isolating: distance yourself from a bad memory

171
Q
emotional lability
disruptive behavior
dec. need for sleep
sexual inappropriateness
auditory hallucinations
Record of previous episodes
A

psychotic feature: auditory hallucination

the record of the previous episode will shift this from a DDx of “bipolar Ds, manic episode with psychotic features”
TO
“Schizoaffective Ds”

172
Q

Schizoaffective Ds

A

mood symptoms
concurrent symptoms of schizophrenia
at least a 2 eek period in the absence of prominent mood symptoms

173
Q

paranoid schizophrenics

A

no mood swings, only paranoia +/-hallucinations

174
Q

Schizophreniform Ds vs. Schizophrenia

A

Both have:
- 2+ of delusions, hallucinations, disorganized speech/behavior +/- (-) Sx

Schizophreniform: Sx longer than 1 month but less than 6

Schizoaffective Ds: 2 weeks of schizophrenic Sx with mood symptoms

175
Q

Tooth crowding
arched palate
long thin face with prominent forehead/jaw
Mental retardation

A

Fragil X Syndrome

CGG Trinucleotide repeat Ds

> 200 = full blown Ds

176
Q

Neurologic deficits that cannot be explained by 1 lesion

motor and sensory

A
suspect MS
Patient is MC a female between 20-30 y/o
- Optic Neuritis
- INO
- Cerebellar DysFx
- Sensory and Motor symptoms: includes bladder and bowel dysfx
177
Q

optic neuritis

A

visual disturbances
Central scotoma
painful eye movements

178
Q

INO

A
Internuclear Ophthalmoplegia (INO)
impaired eye adduction during the lateral gaze during the lateral gaze due to demyelination of the MLF
179
Q

Tremor
Ataxia
Nystagmus

A

Cerebellar DysFx triad

180
Q

MC Non-Specific Symptom of MS

When is this most pronounced and why?

A

Fatigue
- after taking a hot shower or after strenuous activity unheated environments

Due to decreased axonal transmission associated with increased heat.

heat may also lead to worsening of neuro deficits (heat sensitivity)

181
Q

Depression
Apathy
Dementia
Choreiform movements

A

HDx
Progressive
CAG repeat gene

182
Q

Choreiform Movements

A
Facial grimacing
Ataxia
dystonia
tongue protrusion
writhing movements of the extremities
183
Q

transient focal neuro Sx that last less than 24 hrs

A

TIA

184
Q

amaurosis fugax

A

Transient monocular blindeness

In TIA = does not progress to optic neuritis

185
Q

Development of Pruritis when exposed to a hot shower

A

polycythemia

Caused by HIS release from Basophils

186
Q
Neuromuscular excitability
Irregular course tremors
fascicular twitching
agitation 
ataxia
delirium

DDx? Tx? Contraindicated Rx?

A

Chronic Li Toxicity
Gradually develops and will present with neurologic symptoms

Tx: Hemodialysis

contraindicated drugs for Li: 
Thiazide diuretics
ACE-I: impairs CL
NSAIDs: impairs CL
Non-DHPs
187
Q

Lithium

A

Very narrow therapeutic index
Toxicity develops at Cp>=2.0
almost exclusively handled by the kidneys, PCT >60% handling.

Li will impair Na handling, and therefore drop s[Na]. To compensate the kidney tries to take up more Na, but only more Li can come in - this is how you develop Lithium Toxicity

188
Q

What will worsen Lithium toxicity?

A

anything that changes the GFR

  • Renal Injury
  • Toxins
  • Drugs
  • volume depletion
  • decompensated CHF
  • cirrhosis

all will lead to an inc. reabsorption of Li and Na

189
Q

If you have a schizophrenic with HTN and CHF, which drug class should you choose?

A

Furosemide

DHPs (only!)

190
Q

ADDx

Hemangioblastomas

A

VHL
Capillary hemangioblastomas in the Retina/ cerebellum
congenital cysts and/or neoplasms in the:
- Kidney
- Liver
_ Pancreas

Patients are also at risk for bilateral RCC

191
Q

VHL as a TSG

A

VHL controls HIF-alpha phosphorylation. When de-phosphorylated, it can combine with HIF-beta = upreg. of GF: VEGF, PDGF, EDGF, FGF…

192
Q

Von-Recklinghausen’s Dx

A

Chr. 17: NF-1 ADDx
Almost complete penetrance, but variable expressivity

Inherited PERIPHERAL NS tumor syndrome

  • neurofibromas
  • optic nerve gliomas
  • lisch nodules (copper flecks)
  • cafe au lait spots
193
Q

NF-2

A

Neurofibromatosis - 2
ADDx
CNS Tumor syndrome
Bilateral cranial nerve VIII schwannomas and multiple meningiomas

194
Q

Encephalotrigeminal angiomatosis

A

aka Sturge-Weber Syndrome
Rare
Congenital nerucutaneous Ds

195
Q
Facial angiomas
leptomeningioal angiomas
Typically involves V1 and V2 distributions
Mental retardation
Seizures
hemiplegia
Skull radiopacities
Skull = "tram-track" appearance
A

Sturge-weber Syndrome

196
Q

cyts in the kidney

cortial and sub-ependymal hamartomas

A
Tuberous Sclerosis
ADDx
Causes cysts in: 
- kidney
- liver
- pancreas
Also: 
CNS manifestation:
- Hamartomas
Skin: 
- cutaneous angiofibromas
- Visceral cysts
Tuberous Sclerosis is the MCC: 
- Renal Angiomyolipomas
- Cardiac rhabdomyomas
197
Q

Biggest complication in TS

A

Seizures

198
Q
  • epistaxis
  • GI bleeding
  • hematuria
A

Osler-Weber-Rendu Syndomre (HHT)
ADDx of congential telangiectasias
Rupture of the telangiectasias = Sx

199
Q

Waddling Gait

A

Hip instability:

-DMD/ BMD (less)

200
Q

kyphoscoliosis in a young person

A

DMD

Marfan’s

201
Q

lipid accumulation in muscle

A

Carnitine palmitoyltransferase Df

202
Q

Proximal muscle weakness W/O proximal muscle weakness

A

Polymyositis

will show PMN in the myofibers, not near the periphery

203
Q

Ragged Red fibers

A

MESLA

MERA

204
Q

area postrema

A

On dorsal medulla, near the 4th ventricle
Chemoreceptor trigger zone
area that receives blood from fenestrated capillaries, allowing sampling

Thought to be involved in vomiting reflex to toxins/changes in electrolytes

205
Q

ASA (anterior spinal artery)

A
Lateral Corticospinal tract:
Medial Lemniscus
Caudal Medulla (CN XII)
Sx: Contralateral hemiparesis - LE
decreased contralateral proprioception
Ipsilatral hypoglossal dysfunction (tonge deviates ipsilaterally)
Common to present bilatrally
206
Q

MCA stroke

A

Contralateral motor and sensory deficit in face + UE>LE + homonymous hemianopia WITH macular involvement (unlike the PCA which does not have macular involvement)

If Temporal lobe: Wernicke’s Aphasia if in the dominant lobe, hemineglect if in the non-dominant lobe

If Frontal Lobe: Broca’s Aphasia

207
Q

ACA stroke

A

Motor Cortex: Contralateral paralysis of lower limb

Sensory cortex: Contralateral loss of sensation in LE

208
Q

Lateral Striate artery stroke

A

Striatum and internal capsule are affected:

Contralateral hemiparesis/ hemiplegia

209
Q

Common cause of lateral striate artery stroke

A

lacunar infarct (Charcot-Buchard) secondary to HTN

210
Q

which stroke is common bilaterally

A

ASA stroke

211
Q

Medial medullary syndrome

A

infarct of paramedian branches of ASA and vertebral
arteries

Sx:
Contralateral LE hemiparesis with Decreased proprioception (“slapping foot gait”)
Ipsilateral paralysis of the tongue to the ipsilateral side of the lesion (so opposite the LE)

212
Q

Lateral meduallay (Wallenberg’s ) Syndrome

A

Caused by a PICA stroke

“Vomiting, Vertigo, Nystagmus” +

Contralateral Loss of pain and temp sensation
Ipsilateral deficits of:
CN V, VIII, IX, X, XI; and horner’s Syndrome

213
Q

AICA Stroke

A

Classic Sx: Vomiting, Vertigo, Nystagmus and PARALYSIS of the face with preserved touch sensation
Lateral pons: CN nuclei affected
Vestibular nuclei: Vertigo, Vomiting, Nystagmus
Facial Nucleus: decreased taste from anterior 2/3 of the tongue (CN VII),
Spinal Trigeminal nucleus: decreased pain and temp sensation
cochlear nucleus: decreased hearing ipsilaterally
Sympathetic fibers: decreased corneal reflex
Ipsilateral Horner’s Syndrome: decreased lacrimation, salivation (PSNS)

Middle and inferior cerebellar peduncles:
ataxia
dysmetria

214
Q

Lateral Pontine Syndrome

A

Facial nucleus effects are specific to AICA

“If the face droops, then the AICA’s Pooped”

215
Q

sudden onset HA
Partial loss of vision

Contralateral Homonymous hemianopia with macular sparing

A

PCA stroke
occipital cortex, visual cortex
Contralateral hemianopia with macular sparing

216
Q

A. Comm Stroke

A

Common site of saccular (berry) aneurysm = impingement on cranial nerves
leads to visual field defects
Lesions are typically aneurysms, not strokes

217
Q

P.Comm Stroke

A

Common site of saccular aneurysm

CN III palsy

218
Q

“Down and Out”
Ptosis
Pupil dilation

A

CN III palsy

219
Q

“worst HA of your life”

A

Sub-arachnoid hemorrhage

Classically: rupture of a berry aneurysm

220
Q

Berry Aneurysm

A

MCC of Sub A hemorrhage:
At the circle of willis
rupture = SAH: there will be NO focal neuro deficits if it is a SAH
Can see bi-temporal hemianopia with compression of the optic chasm = if still an aneurysm
ADPKD, EDS, Marfans are Genetic disorders classically associated with Berry Aneurysms

221
Q

cuneus vs. lingual gyrus

A

cuneus: upper 1/2 of retina
lingual: lower 1/2 of retina

222
Q

Acute onset
painless
complete loss of vision in one eye

A

Occlusion of the central retinal artery

223
Q

_____ can block tolerance to morphine

A

Ketamine: (-) NMDA (R)

Dextromethorphan: (-) NMDA, reverses tolerance

up-reg glutamate in NMDA (R) which will lead to inc. (P) or inc NO levels, which mediate morphine tolerance

224
Q

NE

  • as a hormone
  • as a NT
A

Hormone: attention and impassivity
NT: post-ganglionic neurons to (+) SNS

225
Q

Innervation to the tongue

A

Motor: CN XII, except the palatoglossus (CN X)
General Sensory:
Anterior 2/3: CN V3
Posterior 1/3: CN IX
Posteror area of the tongue root and taste buds of the larynx and esophagus: CN X
Gustatory:
ant. 2/3: chorda tympani of the CN VII
same for post 1/3 and larynx/esophagus as it is for sensory

226
Q

terminal sulcus and foramen cecum of the tongue

A

Think of an Arrow:
terminal sulcus is the front full edge (triangle), the foramen cecum is the tip.
the wood stick and back is going to be the anterior 2/3 of the tongue and is innervated by CN XII, V3, and the chorda tympani of the VII for motor, sensory, and taste, respectively

227
Q

+/- history of aneurysm
AMS (+)
neurological deficits

DDx? Tx?

A

Vasospasm post sub-A hemorrhage

Treat with Nimodipine

228
Q

generalized muscle stiffness
shaking of one hand
3 weeks ago he had a psychotic episode

A
Drug-induced parkinsonism
- D2 (R) (-)
Anti-Psychotics: T>A
(Haloperidol is the most)
Anti-emetics/ GI motility agents:
Prochorperazine, metoclopramide

Sx: Prominent rigidity & bradykinesia
Tremor at rest and postural
Masked facies

Tx: dec. / stop Rx, Anti-cholinergics (Trihexyphenidyl, benztropine), Amanatadine (anti-viral with (+) DA)

229
Q

Trihexylphenidyl

Benztropine

A

used to reverse Drug induced parkinsonism

these are CNS acting anti-Mx(R)

230
Q

In what time period would it make sense to suspect Drug induced parkinsonism

A

first 3 mod of Tx

231
Q

Person comes in with Drug induced Parkinsonism - give him Levodopa right?
Bromocriptine?

A

No - it can precipitate psychosis

232
Q

In what patient population are trihexyphenidyl and benztropine contraindicated?

A
  • elderly
  • closed - angle glaucoma
  • BPH

can also cause dry mouth and suppurative parotitis

233
Q

Used to Tx:
Seizures
Anxiety Disorders
Muscles Spasms

A
Benzodiazepine:
Diazepam
modulates GABA-A (R)
CNS depressant with significant abuse potential
Drug abuse Sx:
Mild euphoria
relaxation
mild amnesia
sedation
slurred speech
dec. RR, BP, HR
234
Q

Indications:

Akathisis

A

Propanolol - beta blocker

235
Q

Hemiballismus

A

contralateral sub-thalmic nucleus

damage MC due to lacunar stroke

236
Q

classic patient that has lacunar stroke

A

long-standing poorly controlled HTN

237
Q

Subthalamic nucleus is located:

A

ventral to the thalamus, superior to the internal capsule

238
Q

Wing-beating tremor
Psychosis
Cirrhosis
Kayser-Fleischer rings in cornea

A
Wilson Disease:
Lentiform nucleus (globus pallidus + putamen)
239
Q

a pure motor or pure sensory deficit would be expected to be localized at _____

A

the internal capsule= when perf. A are obstructed

240
Q

Thalamic syndrome

A

burning on one half of the body post thalamic stroke

241
Q

“Red Neuron”

A

Transient severe ischemia, hypoxia, toxicity damage that leads to neuronal cell death

Not seen with normal aging - that would be apoptosis

242
Q

MCC of metabolic encephalopathy

A

hypoglycemia
hyperglycemia
hepatic encephalopathy (ammonia toxicity)

243
Q

Lisch nodules

A

Hamartomas of the iris: NF-1

Hamartomas of the cornea: Wilson Disease

244
Q

Nml division of the prosencephalon

A

5th week of development

245
Q

Holoprosencephaly is associated with what three conditions:

A
Trisomy 13 (Patau's syndrome)
Trisomy 18 (Edward's Syndrome)
FAS
246
Q

loss of GABA in the brain

A

HDx

247
Q

NO in the brain has a unique job - what is it?

A

formation of new memories - communication between FC, hippocampus, hypothal, cerebellum, olfactory bulb

248
Q

HDx gene - chr.?

A

4

249
Q

Indications:
Absence Sz
Tonic-clonic Sz

In children

A

Valproate

250
Q

Indications:

Absence Sz in children

A

Ethosuximide

VSCC - T- Type (-)

251
Q

Indications:
Tonic-Clonic Sz
Status Epilepticus

A

Phenytoin

VSSC (-)

252
Q

Indications

tonic-clonic Sz

A

Phenobarbitol

253
Q

Indications:
Complex Partial Sz
Tonic-Clonic

Adverse Effect?

A

Carbamazepine

AE: Agranulocytosis, Aplastic Anemia

254
Q

Drugs that cause agranulocytosis

A

Clozipine

Carbamazepine

255
Q

Drugs that cause Aplastic anemia

A

Carbamazepine

256
Q

Ischemic-Hypoxic encephalopathy (aka global cerebral ischemia)

A

You are going to hit your watershed zones and those will go ischemic first.
Borders between the ACA, MCA, and PCA.

ACA-MCA watershed: Frontal lobe about 15 degrees from midline

MCA - PCA watershed: posterior temporal lobe between the occipital/ temporal lobes
these will display wedge shaped infarcts

257
Q

Loss of O2 to the brain for:

A. 5-10 sec.
B. 1+ min.
C. 4-5 min.
D. Areas hit first
E. Areas hit second
A
A. LOC (syncope)
B. stop neuron activity
C. permanent damage
D. Most sensitive cell groups: Purkinje cell layer of the cortex (5,6), purkinje layer of the cerebellum, and the pyramidal cells of the hippocampus. 
E. Watershed zones
258
Q

mu (R) traits

A
  • physical dependence
  • Euphoria
  • Respiratory and cardiac depression
  • Sedation
259
Q

Kappa (R) traits

A

Miosis
dysphoria
sedation

260
Q

delta (R) traits

A

Anti-depressant effects

261
Q

Nociception/ orphanin (N/OFQ)

A

Anxiolysis

Increased appetite

262
Q

Naloxone

A

pure -opioid receptor antagonist with the greatest affect at mu (R)
used to pull people off of opioid overdose

Reversal seen in min.

duration is dose-dependent (keep them on a drip - you don’t need them to go back under because the drug hasn’t cleared yet)

It must be given IV because it is inactivated in the liver

263
Q

Hexamethonium

A

potent nicotinic receptor antagonist

264
Q

Phencyclidine (PCP)

A
Hallucinogen: NMDA (R) (-) = excess relase of (+) NT
Sx: 
Agitation 
DISSOCIATION: Medium dose
VIOLENT BEHAVIOR: High dose

PE:
NYSTAGMUS
ataxia
memory loss

265
Q

Cocaine

A
Stimulant: (-) catecholamine reuptake
Sx:
Euphoria
Increased arousal
agitation
CHEST PAIN
HA
SEIZURES
PE:
Tachycardia
HTN
MYDRIASIS
the word is longer, so its a blown pupil

MI/Stroke: Serious complications due to severe vasoconstriction

Acute intoxication lasts for less than 1 hour.

266
Q

Methamphetamine

A
Stimulant: 
intoxication lasts 20 minutes (longer than PCP)
Sx: 
agitation
PSYCHOSIS
diaphoresis
violent behavior
PE: 
Tooth decay
HTN
Tachycardia
Choreiform movement
267
Q

LSD

A
Hallucinogen
Very unpredictable drug
Sx: 
VISUAL HALLUCINATIONS
depersonalization
Euphoria
occasional dysphoria
panic

PE:
Mild tachycardia
mild HTN
ALERT AND ORIENTED

268
Q

Marijuana

A
Psychoactive Drug
Sx: 
increased appetite
euphoria
slowed reflexes
impaired time perception

PE:
Dry mouth
conjunctival injection
mild tachycardia

269
Q

Heroin

A
Opioid Analgesic:
Sx: 
Mild euphoria
lethargy
coma

PE:
MIOSIS
DECREASED RR - life threatening
DECREASED BOWEL SOUNDS

Don’t be fooled - the BP/HR can be NML to low

270
Q

Somatozation Dx

A
Somatoform Ds
Pts. with numerous physical complaints over the course of years with no physical cause. 
Must have started prior to 30yo
significant impact on social/occupational Fx
Must have at least:
- 4 pain symptoms
- 2 GI symptoms
- 1 sexual problem
- 1 pseudoneurologic Sx
271
Q

Ptosis, Miosis, Anhydrosis, Enophthalmos

A

Horner’s Syndrome
Ipsilateral interruption of SNS due to impingement (i.e. tumors in the apex of the lung (adenocarcinoma), Pancoast tumors):
1. Partial Ptosis due to denervation of the SNS controlled Muller muscle of the upper eyelid
2. Miosis: SNS fibers are interrupted on their way to the dilator pupillage muscle, = unopposed PSNS
3. anhydrosis: impaired sweating due to no SNS innervation to face
4. enophthalmos - opposite of exophthalmos

With further invasion/ compression, there will be impingement of the brachial plexus = ipsilateral shoulder and arm pain
Compression of the SCA = UE edema

272
Q
Ipsilateral paralysis of: 
soft palate
pharynx
larynx
hoarseness
dysarthria
dysphagia
loss of gag reflex
A

CN X compression

273
Q

synaptophysin

A

protein on pre-synaptic vesicles of neurons, neuroendocrine, and neuroectodermal cells.

274
Q

CNS tumors will frequently stain (+) for:

A

Synaptophysin

275
Q

Glial CNS tumors will always stain (+) for:

A

GFAP (+)
astrocytomas
ependymomas
oligodendrogliomas

276
Q

sudden onset left eye pain that has lasted for 30 minutes then resolved spontaneously.
+
Jaw pain that starts in the middle of a meal

A

Giant Cell Temporal Arteritis

will cut off circulation to the working muscles of mastication (and tongue claudication is actually a thing)

presents in the elderly
MC Sx: HA
scalp tenderness, especially during hair combing
inflamed temporal artery can sometimes be palpated as firm painful subcutaneous cord in the temporal region

50%: polymyalgia rheumatica that is worse in the mornings

When the suspicion is high - check ESR, if elevated - DO NOT WAIT FOR BIOPSY - START ON PREDNISONE LEST THEY LOSE AN EYE.

The ESR will always be high

277
Q

Jaw claudication +

ESR > 1000mm/hr

A

giant cell temporal arteritis

278
Q

delirium

A

acute onset mental status change in the setting of a medical condition
- causes global memory impairment with fluctuations of consciousness.

When considering delirium as a DDx look for things that would either (a) change the electrolyte balance (i.e. dialysis) or (b) infection

279
Q

ADx

A

irreversible and progressive memory loss that leads to compromise in all facets of life.
this will develop over the course of years
Remote memory is initially spared, and there is never a loss of consciousness

280
Q

breif psychotic disorder

A

pschyotic symptoms that last for a few hours - month

the patient will return to the same pre-morbid state that he was once the episode concludes

281
Q

Vascular dementia

A

(aka Multi-infarct dementia)

Additive effects
will have (+) focal neurologic deficits
282
Q

Delirium vs. Dementia

A

Onset: Acute Vs. Gradual
Consciousness: Impaired vs. intact
Course: Waxing and Waning vs. additive and progressive
Prognosis: reversible vs. irreversible
Memory impairment: global vs. remote memory is spared

283
Q

On Histology:

  1. cell body rounding
  2. displacement of nuclei
  3. dispersion of the Nissl Substance

what happened?

A

axonal section and reaction

when an axon is severed there is “Wallerian degeneration”: degeneration of axon and myelin distal and proximal to the site of injury

284
Q

Wallerian degeneration

A
  • occurs where a segment of axon is separated from the soma
  • 1- swelling and irregularity in the distal axon
  • 2- w/in 1 week the axon is destroyed
  • 3- fragments are digested by schwann cells and M0

this degeneration is bidirectional

285
Q

What changes occur in the neuronal cell body seen after an axonal section?

A

AXONAL REACTION

  1. cellular edema
  2. swollen, rounded, with the nucleus displaced to the periphery
  3. Nissl substance becomes fine, granular, and is dispersed throughout the cytoplasm (aka central chromatolysis)
286
Q

When does “axonal reaction” become visible

A

24-48 hrs post injury
Maximal changes in the neuronal body occur ~ 12 days post-injury.

this increased change represents a high turn over of protein in order to regenerate the axon.

287
Q

irreversible cell injury will be seen as__?

A

Hypoxia/ ischemia/ toxic injury will show:

  1. shrunken cell
  2. pyknotic nucleus
  3. deeply eosinophilic cytoplasm
  4. LOSS of Nissl substance
288
Q

in terms of nissl substance, how can you differentiate an axonal reaction vs. apoptosis due to ischemic cell injury?

A

the nissl substance is lost in ischemic injury. it is just disbanded in axonal injury

289
Q

loss of size and number of neurons would indicate that there was___?

A

compression atrophy

mass affect, ICP

290
Q

infarcts of the anterior pons will affect what tracts?

A

corticospinal (pyramidal) tracts

corticobulbar tracts

pontine nuclei and pontocerebellar fibers

291
Q

damage to the corticospinal tracts at the level of the pons =

A

CL hemiparesis and (+) babinski sign

292
Q

damage to the corticobulbar tract

A

CL facial palsy and dysarthria

293
Q

damage to the pontine and pontocerebellar fibers during damage to the pons

A

Ataxic hemiparesis:

  • CL dysmetria
  • CL dysdiadochokinesisa

part of cerebellar processes

294
Q

difference between a lesion in the cerebellum and the pons?

A

in the cerebellum = ipsilateral deficit
in the pons = contralateral deficit at the basis pontis because at this level the fibers enter the cerebellum enter via the CL peduncle

295
Q

what is the only CN that will present with a contralateral deficit?

A

the trochlear nerve - the only once to decussate before innervating its target.

296
Q

Causes of Conductive hearing loss

A
  • Cerumen impaction
  • Cholesteatoma
  • Otosclerosis
  • External or middle ear tumors
  • Tympanic membrane rupture
  • severe otitis media
297
Q

Causes of senorineural hearing loss

A
  • congenital
  • Meniere’s Dx
  • ototoxic drugs
    (i. e. aminoglycosides)
298
Q

ototoxic drugs

A

Aminoglycosides

299
Q

Abnormal rinne test means that:

A

bone > air

conductive hearing loss

300
Q

Abnormal Weber Test

A

the sound will localize to the affected ears, instead of being even in both ears:
conductive

301
Q

Conductive hearing loss

A

a problem in the sound transduction mechanism, but not reception.

causes lateralization to the affected are as the conduction deficit masks the ambient noise in the room

302
Q

sensorineural hearing loss

A

will cause laterlization to the unaffected ear as the unimpaired inner ear can better sense the vibration

303
Q

Low Potency Typical Antipsychotic medication:

A

Sedation (H1 block)
Anti-ACh effects (ACh block)
Orthostatic Hypo-TN (alpha-1 block)

Ex:
Chlorpromazine
Thiroidazine

304
Q

High Potency Typical Antipsychotic drugs:

A
EPSx: Due to D2 block
Acute Dystonia
Akathisia
Akinesia
Parkinsonism

Ex:
Haloperidol
Fluphenazine

305
Q

Hyperglycemia as an anti-psychotic Rx - Most likely what class?

A

Atypical

it is the most with Olanzapine

306
Q

tabes dorsalis

A

due to tertiary neurosyphilis
occurs in < 10%
longest latency period, occurring 20-30 years post primary infection

spirochetes target the sensory dorsal roots, and eventually demyelinate and cause axonal damage in the DCML

307
Q
Lancinating pains
paresthesias
loss of vibratory and position sense
arreflexia
Argyll Robertson pupils
(+) romberg sign
A

Loss of proprioception is compensated by visual cues - however with loss of night time vision - there will be stumbling

308
Q

argyll robertson pupils

A

HIGHLY SPECIFIC SIGN FOR NEUROSYPHILIS

pupils that are non-reactive to light but will constrict during accommodation

309
Q

Meckel’s diverticulum: Cause

how many GI layers

A

Failure to obliterate the omphalomesteric duct.

Has all three layers:
Mucosa, Submucosa, and Muscularis

310
Q

Meckel’s diverticulum: MC presentation

A

Painless Melena or with intestinal obstruction that causes RLQ pain

Bloody stools that are dark are due to the gastric acid that is being secreted into the lower GI tract (where it doesn’t belong)

311
Q

An inflamed Meckel’s diverticulum can mimic___

A

Appendicitis

312
Q

colicky Abd. pain

“Red Current Jelly Stools”

A

Intussusception

313
Q

Imperforate anus

A

Failure of Hindgut formation/ malformation

314
Q

Neonate
failure to pass meconium
Bilious vomiting
Abd. distention

A

Hirschprung’s Disease

315
Q

MC Rx that cause ED

A
SSRIs
SNS blockers (clonidine, methyldopa, BB)
316
Q

MC traumatic causes that lead to ED

A

Recent pelvic trauma
Prostate surgery
Priapism

317
Q

MC met to the ovary

A

Gastric CA

“Krukenburg Tumor”

318
Q

Krukenburg tumor
Sister-Mary-Joseph Nodule
Virchow’s node

A

Metastasis of Gastric CA

319
Q

Periodic, Non-peristaltic contractions of the esophagus

A

Diffuse Esophageal Spasm (DES)

Several segments will contract at the same time, preventing peristalsis

Often painful (can mimic angina pectoris). Differentiated because the chest pain is not associated with exertion, and is not resolved by rest.

320
Q

Pleuritic Chest pain
coughing
dyspnea
hemoptysis

A

PE

321
Q

RUQ pain
Radiation to back/neck
worse with meals

A

cholecystitis

may also see:
fever
nausea
vomiting

322
Q

Hydrocele

A

Collection of peritoneal fluid within the tunica vaginalis

the peritoneal tissue = processus vaginalis - if this fails to obliterate = increased risk for hydrocele that can even move up into the abdomen

323
Q

HNPCC I vs. II

A

HNPCC I: Adenocarcinoma of the colon < 50 yo
HNPCC II: HNPCC I that can co-present (in same person or in family tree) with endometrial and ovarian CA, Stomach CA, Pancreatic CA, or urothelial tract + others

324
Q

Cirrhosis
Kayser-Fleisher Rings
CNS involvement

A

Wilson’s disease

325
Q
cirrhosis
pancreatic fibrosis
DM
cardiomyopathy
secondary hypogonadism
A

Hemochromatosis

326
Q
Urinary Retention
Prolonged QRS/QT interval
SZs
Orthostatic Hypotension
Tyramine Reaction
Sedation
Depression Rx
A

TCADs

327
Q

clomipramine has a high side effect of:

A

SZs

it is a TCAD

328
Q
patient is admitted for \_\_\_\_ badness\_\_\_. 
next day presents with:
- disorientation
- abdominal distention
- flapping tremor (asterixis)
- gynecomastia
- decreased liver span
A

Hepatic encephalopathy

329
Q

What mediates all the symptoms of Hep. B infection, EXCEPT the hepatic s/sx

A

Immune complex deposition

330
Q
sterility
thick mucous in lungs
pancreatic insufficiency
Mucous plugging of biliary ducts (leads to obstructive biliary cirrhosis), and salivary ducts
Frequent URIs
Bilateral sinusitis
Nasal polyps
A

CF

331
Q
Calcinosis
Raynaud's (can lead to fingertip ulceration)
Esophageal dymotility
Sclerodactyly
Telangeictasia
A

CREST Syndrome
(+) anti-mitochondrial Ab.
Systemic sclerosis that involves the skin of the face and fingers

CD4 cells are induced to produce tons of collagen = excessive tissue fibrosis

Esophageal dysmotility is a resutlt of atrophy and fibrous replacement of esophageal muscles, and the LES will become atonic and dilated = severe reflux

332
Q

Hepatomegaly
Abdominal pain
Ascites
Liver is grossly swollen, reddish purple with a TENSE capsule

A

Budd-Chiari Syndrome

Severe centrilobular congestion and necrosis are present

we are really worried about these patients getting in any hard contact in the liver = can break the capsule = hemorrhage

333
Q

Normal liver with signs of portal HTN

A

pre-cirrhotic pathology
clot in the portal vein before the liver.

Ascites is uncommon, but esophageal ruptured varices are common

334
Q

Fibrates inhibit what enzyme

A

7-alha-hydroxylase

inhibits the production of cholesterol to bile salts, which has the potential to lead to cholesterol stones

335
Q

epigastric pain
vomiting
EtOH in PSH

DDx: Pancreatic pseudocyst

MCL:

A

MCL: lesser peritoneal sac - bordered by the stomach, duodenum and transverse colon.
it will be posterior to the stomach