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STEP1 > Patho > Flashcards

Patho Flashcards

1
Q

Apolipoprotein C-II deficiency

A

1 (Hyperchylomicronemia)

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2
Q

breaks down the triglycerides in chylomicrons and VLDL to form LDL.

A

Apolipoprotein C-II

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3
Q

elevated levels of chylomicrons, triglycerides, and cholesterol.

A

1 (Hyperchylomicronemia)

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4
Q

Cofactor for lipoprotein lipase

A

Apolipoprotein C-II

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5
Q
  • Pancreatitis from elevated triglycerides
  • Eruptive xanthomas
  • No increased risk of atherosclerosis
  • Hepatosplenomegaly
A

1 (Hyperchylomicronemia)

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6
Q
  • Accelerated atherosclerosis

* Achilles tendon xanthomas

A

2 (Hypercholesterolemia)

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7
Q

Low-density lipoprotein receptor or apolipoprotein B-100 deficiency

A

2 (Hypercholesterolemia)

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8
Q

2 (Hypercholesterolemia)

Cause:

A

Low-density lipoprotein receptor or apolipoprotein B-100 deficiency

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9
Q

Accelerated atherosclerosis

Achilles tendon xanthomas

A

2 (Hypercholesterolemia)

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10
Q

Premature atherosclerosis

Palmar xanthomas

A

3 (Dysbetalipoproteinemia)

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11
Q

3 (Dysbetalipoproteinemia)

Cause:

A

Apolipoprotein E deficiency

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12
Q

Clearance of lipoprotein and chylomicron remnants from circulation

A

Apolipoprotein E

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13
Q

Mutations are associated with late-onset Alzheimer disease

A

Apolipoprotein E

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14
Q

Overproduction of very low–density lipoprotein

A

4 (Hypertriglyceridemia)

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15
Q
  • Pancreatitis from elevated triglycerides

* Related to insulin resistance

A

4 (Hypertriglyceridemia)

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16
Q

Required for the assembly and secretion of chylomicrons

A

B-48

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17
Q

Structural protein for high-density lipoprotein

Activation of lecithin acyltransferase

A

A-1

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18
Q

Apo E mediates remnant uptake menos del

A

LDL

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19
Q

Found only on alpha lipoproteins

A

A-1

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20
Q

Binds LDL receptor

Solo esta en particulas que se originan del intestino

A

B-100

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21
Q

Arterial bleeding between skull and dura

A

no cruza la linea media
da “periodo lucido”

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22
Q

Ruptura de un aneurisma

A

subarachnoid hemorrhage (SAH)

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23
Q

Slow bleeding de un bridging cerebral vein

A

between the dura and arachnoid maters

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24
Q

disruption of the middle meningeal artery.

between skull and dura

A

epidural hematoma

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25
Q

small-vessel vasculitis (2)

A
  • Granulomatosis with polyangitis (also known as Wegener disease)
  • Mixed cryoglobulinemia
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26
Q

large arteries vasculitis

A

Takayasu arteritis.

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27
Q

Medium-vessel vasculitis

A

Polyarteritis nodosa

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28
Q

chronic sinusitis, otitis media, and/or perforation of the nasal septum in addition to hemoptysis, cough, and/or dyspnea + Hematuria

A

Granulomatosis with polyangitis (also known as Wegener disease)

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29
Q

Type of Renal involvement in Granulomatosis with polyangiitis (Wegener disease)

A

crescentic glomerulonephritis

Hematuria

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30
Q

Type of ANCA in Granulomatosis with polyangiitis (Wegener disease)

A

C-ANCA

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31
Q

Type of ANCA in Microscopic Polyangitis

A

p-ANCA

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32
Q

Asthma,Recurrent sinusitis,Purpuric skin lesions,,Polyneuropathy, often wrist or foot drop
***Renal involvement is rare!

A

Eosinophilic Granulomatosis With Polyangitis

Churg-Strauss syndrome

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33
Q

Granulomatous, necrotizing inflammation in small-sized arteries

A

Eosinophilic Granulomatosis With Polyangitis

(Churg-Strauss syndrom

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34
Q
  • Focal necrotizing vasculitis in small-sized arteries
  • Necrotizing granulomas in the lung and upper airway
  • Necrotizing glomerulonephritis
A

Granulomatosis With Polyangitis

Wegener disease

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35
Q

LABS in Wegener disease

A
  • C-ANCA
  • No eosinophilia
  • Red blood cast in urine
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36
Q

Necrotizing vasculitis without granulomas

A
  • Microscopic Polyangitis

- P-ANCA

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37
Q

-Adenocarcinoma (eg, lung, ovary)
-Lung cancer
-Breast cancer
-Lymphoma
Paraneoplastic Syndrome:

A

Dermatomyositis and polymyositis

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38
Q

Involved Site: Dermatomyositis and polymyositis

A

Muscle fibers

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39
Q

Dermatomyositis and polymyositis

Pathophysiology->

A

Dermatomyositis → perimysial inflammation (CD4+ T cells)

Polymyositis → endomysial inflammation (CD8+ T cells)

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40
Q

Autoimmune → anti–Jo-1, anti–Mi-2, and anti-SRP

A

Dermatomyositis and polymyositis

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41
Q

Symmetric proximal muscle weakness,Normal deep tendon reflexes,Gottron papules, heliotrope violaceus rash)

A

Dermatomyositis and polymyositis

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42
Q

Presynaptic membrane voltage-gated calcium channels

A

Lambert-Eaton myasthenic syndrome (LEMS)

*Small-cell lung cancer

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43
Q

Autoimmune → anti-calcium channel antibodies

A

Lambert-Eaton myasthenic syndrome (LEMS)

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44
Q

Proximal muscle weakness that improves with use
Autonomic dysfunction
↓ or absent deep tendon reflexes

A

Lambert-Eaton myasthenic syndrome (LEMS)

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45
Q

Myasthenia gravis ass

A

Thymoma

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46
Q

Acetylcholine receptor in postsynaptic membrane

A

Myasthenia gravis

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47
Q

Autoimmune → anti-acetylcholine receptor antibodies

A

Myasthenia gravis

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48
Q

Muscle weakness that worsens with use
Ocular symptoms → ptosis, diplopia
Bulbar symptoms → dysphagia

A

Myasthenia gravis

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49
Q

decreased generation of thrombin at the end of the coagulation cascade

A

Hemophilia

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50
Q

X-linked ↓ factor VIII

A

Hemophilia A

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51
Q

X-linked ↓ factor IX

A

Hemophilia B

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52
Q

key feature suggestive of hemophilia

A

isolated abnormal aPTT

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53
Q

Impaired inactivation of factor V

A

factor V Leiden disorder

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54
Q

prone to the development of deep vein thromboses

A

factor V Leiden disorder

** patients with calf or proximal thigh tenderness

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55
Q

von Willibrand disease (vWD)

A

defective or reduced levels of von Willibrand factor (vWF), which is an extracellular matrix protein that allows platelet adhesion during initiation of primary hemostasis.

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56
Q

Vitamin K is required for the synthesis of factors

A

II, VII, IX, and X and proteins C and S

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57
Q

Hereditary Platelet Disorders: (2)

A
  • Bernard-Soulier Syndrome

- Glanzmann Thrombasthenia

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58
Q 
↓ glycoprotein Ib 
↓ platelet-to-von Willibrand factor adhesion
Large platelets
Bleeding time increased
Platelet count normal or decreased
A

Bernard-Soulier Syndrome

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59
Q 
↓ glycoprotein IIb/IIIa
↓ platelet-to-platelet aggregation
↓ platelet plug formation
Shows no platelet clumping
Bleeding time increased
Platelet count normal
A

Glanzmann Thrombasthenia

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60
Q

forming very low–density lipoprotein (VLDL)

A

Apo B-100

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61
Q

Cholesterol is synthesized by the liver by:

A

HMG-CoA reductase

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62
Q

Statins MOA

A

By blocking the synthesis of cholesterol, statins deplete intrahepatic cholesterol. The liver subsequently upregulates LDL receptor expression in an attempt to absorb more circulating LDL and replenish intrahepatic cholesterol. The ultimate result is lower circulating LDL

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63
Q

Most specific for diagnosing hereditary spherocytosis

A

-Gold-standard is osmotic fragility test

↓ mean fluorescence in eosin 5-maleimide binding test

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64
Q

Defective ankyrin and/or spectrin → RBC cytoskeleton defects

A

hereditary spherocytosis

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65
Q

Treatment -> hereditary spherocytosis

A

Splenectomy

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66
Q

Complications-> hereditary spherocytosis

A

Aplastic crisis with parvovirus B19

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67
Q

peripheral blood smear findings in hereditary spherocytosis

A

On peripheral blood smear, spherocytes and/or Howell-Jolly bodies may be seen.

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68
Q

Test reveal an absence of CD55 and CD59

A

Paroxysmal nocturnal hemoglobinuria (PNH)

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69
Q

hemolytic anemia, pancytopenia, and large vein thrombosis (often in the hepatic vein)

A

Paroxysmal nocturnal hemoglobinuria (PNH)

**may complain of dark urine in the morning.

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70
Q

binds to free hemoglobin and, therefore, will be decreased in patients with hemolytic anemia

A

Haptoglobin

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71
Q

presence of hemoglobin A2 levels > 3.5%

A

β-thalassemia minor

** microcytic anemia (mean corpuscular volume < 80 μm3)

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72
Q

Seen in patients post splenectomy or in patients with splenic dysfunction (eg, sickle-cell disease,asplenia,hyposlenia hereditary spherocytosis)

A

Howell-Jolly bodies

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73
Q

Seen in patients with macrocytic, megaloblastic anemia secondary to folate deficiency, vitamin B12 deficiency, or orotic aciduria.

A

Hypersegmented neutrophils

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74
Q

increased RDW is seen in patients with

A

hereditary spherocytosis, iron deficiency anemia, and macrocytic anemia secondary to folate and vitamin B12 deficiency.

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75
Q

Note that spherocytes (and microspherocytes) may also be seen in patients with

A
  • autoimmune hemolytic anemia
  • glucose-6-phosphate dehydrogenase deficiency
  • Hereditary spherocytosis
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76
Q

Chronic Lymphocytic Leukemia Typically affects

A

older patients

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77
Q

peripheral smear will show numerous “smudge” cells

A

Chronic Lymphocytic Leukemia

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78
Q

Chronic leukemias C/Fx

A

-Inicio insidioso (fatiga > 5 meses) + palpable lymph nodes+ Normocytic anemia and thrombocytopenia.

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79
Q

Auer rods are found in the cytoplasm of myeloblasts

A

acute myelogenous leukemia

**most notably acute promyelocytic leukemia (APL)

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80
Q

APL often develops in

A

young to middle-aged

**sudden bleeding gums and multiple ecchymoses

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81
Q

acute promyelocytic leukemia (APL) commonly associated with the translocation of chromosome

A

t(15;17)

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82
Q

APL often associated with

A

disseminated intravascular coagulation

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83
Q

Leukemic cells with hair-like projections describe

A

hairy cell leukemia

uncommon B cell leukemia.

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84
Q

commonly older males with MASSIVE splenomegaly and who have pancytopenia (NO Leukocitosis)

A

hairy cell leukemia

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85
Q

hairy cells are

A

tartrate-resistant acid phosphatase positive and also exhibit CD11c and CD103

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86
Q

Numerous lymphoblasts on peripheral smear are typically seen with

A

acute lymphoblastic leukemia (ALL)

**greater than 20% blasts on the peripheral smear and in the bone marrow

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87
Q

ALL usually develops in

A

children

**fever without evidence of infection is the most common symptom. Patients can also have bleeding from thrombocytopenia.

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88
Q

Pencil cells are characteristic of

A

iron deficiency anemia

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89
Q

Acute Lymphoblastic Leukemia T-Cell can present with:

A

mediastinal mass: dysphagia, dyspnea, superior vena cava syndrome

90
Q

Chronic Myelogenous Leukemia Translocation

A

9;22

91
Q

IL-1 Secreted by What Cells

A

Macrophage

92
Q

Induces fever
Induces adhesion molecule expression in endothelial cells
Induces secretion of other cytokines

A

IL-1

93
Q

IL-1

A

Induces fever
Induces adhesion molecule expression in endothelial cells
Induces secretion of other cytokines

94
Q

IL-2 Secreted by What Cells

A

All T cells

95
Q

Induces differentiation of immature T cells into regulatory, cytotoxic, and helper T cells

A

IL-2

96
Q

IL-3 Secreted by What Cells

A

All T cells

97
Q

Induces differentiation and growth of immature bone marrow stem cells

A

IL-3

98
Q

Induce isotype switching for IgG and IgE production

A

IL-4

99
Q

IL-5 Secreted by What Cells

A

T helper type 2 cells

100
Q

IL-4 Secreted by What Cells

A

T helper type 2 cells

101
Q

Induce isotype switching for IgA production and promote eosinophil differentiation/proliferation

A

IL-4

102
Q

IL-6 Secreted by What Cells

A

Macrophage

103
Q

Stimulates production of acute phase reactants

A

IL-6

104
Q

IL-8 Secreted by What Cells

A

Macrophage

105
Q

Chemokine for neutrophils

A

IL 8

106
Q

IL-10 Secreted by What Cells

A

T helper type 2 cells

107
Q

Attenuates inflammation
Decreases MHC II and Th1 cytokine expression
Inhibits activated macrophages and dendritic cells

A

IL-10

108
Q

Promotes differentiation of Th1 cells

A

IL-12

109
Q

IL-12 Secreted by What Cells

A

Macrophage

110
Q

Induces macrophage activation, inhibits Th2 differentiation

A

IFN-γ

111
Q

IFN-γ Secreted by What Cells

A

T helper type 1 cells

112
Q

WBC recruitment and vascular permeability

A

TNF-α

113
Q

TNF-α Secreted by What Cells

A

WBC recruitment and vascular permeability

114
Q

has a role inhibiting leukotriene production

A

prostaglandin E2

115
Q

aspirin-exacerbated respiratory disease (AERD)

MOA

A

aspirin blocks the cyclooxygenase enzymes, the arachidonate precursors are prevented from forming prostaglandins. Prostaglandin E2 has a role inhibiting leukotriene production; therefore, the lower levels of prostaglandin E2 could be responsible for the excess leukotrienes. The excess leukotrienes create a state of chronic lung inflammation

116
Q

acute phase reactants stimulated by IL-6 include:

A

_Ferritin

  • C reactive protein
  • Serum Amyloid A
  • Fibrinogen
  • Cerulosplasmin
117
Q

Activates macrophages and plays an important role in granuloma formation.

A

IFN-γ

118
Q

Conditions That Cause eosinophilia->
Immunologic disorders
(3)

A
  • Job syndrome (Hyper-IgE Syndrome)
  • Idiopathic hypereosinophilic syndrome
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
119
Q

Conditions That Cause Eosinophilia -> Allergic Disorders

A 
Asthma
Allergic rhinitis
Atopic dermatitis
Drug Rash with Eosinophilia and Systemic Symptoms syndrome
Acute interstitial nephritis
120
Q

Conditions That Cause Eosinophilia-> Infectious Disease

A
  • Helminths
  • Chlamydial pneumonia
  • Allergic bronchopulmonary aspergillosis
121
Q

medications that should be given to patients that present with signs of labor prior to 37 weeks’ gestation.

A
  • Bethamethasona ->stimulate surfactant production

- Tocolytics -> terbutaline (b2 agonist)

122
Q

Consequences of Renal Failure

A

MAD HUNGER
MA: Metabolic Acidosis
D: Dyslipidemia (incressed tryglicerides)
H:High Potassium
U:Uremia-> axterexis,encephalopaty,pericarditis,platelet dysfunction.
N: Na+/H2O retention -> Heart failure,Hypertension,Pulmonary edema
g: growth retardation
E: erythropoietin failure
R: Renal osteofystrophy (hypocalcemia,hyperphosphatemia,subperiosteal thinning of the bones)

123
Q

Skin findings -> Sarcoidosis

A

lupus pernio, a purple discoloration of the nose and cheeks

124
Q

Increased Anion Gap Metabolic Acidosis

A 
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or isoniazid
Lactic acidosis
Ethylene glycol
Salicylates (late)
125
Q

Normal Anion Gap Metabolic Acidosis

A

HARDASS

Hyperalimentation or hyperchloremia
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
126
Q

Commonly tested causes of lactic acidosis include:

A

Cyanide toxicity
Diabetic ketoacidosis
Glucose-6-phosphate deficiency (Von Gierke disease)
Metformin
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
Regional hypoperfusion (eg, skeletal muscle hypoxia post-stroke, bowel ischemia)
Sepsis
Shock
Tumor lysis syndrome

127
Q

postictal lactic acidosis. Tonic-clonic seizures

A

increased anion gap metabolic acidosis-> skeletal muscle hypoxia

128
Q

Formula Anion GAP

A

Anion gap = Na+ - [Cl- + HCO3-]

normal anion gap is 8-12 mEq/L

129
Q

Type 1 RTA

A

characterized by insufficient production of new bicarbonate

130
Q

type 2 RTA

A

characterized by defective bicarbonate reabsorption in the proximal convoluted tubule (PCT) and increased excretion of bicarbonate in the urine.

131
Q

VHL disease (inherance)

A

HAD

VHL gene on chromosome 3

132
Q

Tumors seen with VHL disease include:

A

Pheochromocytoma
Hemangioblastomas in the retina, brain stem, cerebellum, and spine
Angiomatosis (ie, cavernous hemangiomas in the skin, mucosa, and organs)
Bilateral renal cell carcinomas

133
Q

marfanoid body habitus, mucosal neuromas, medullary thyroid carcinoma, and pheochromocytoma

A

MEN2B

134
Q

parathyroid hyperplasia, medullary thyroid carcinoma, and pheochromocytomas

A

MEN2A

135
Q

Both MEN2A and MEN2B are caused by mutations

A

RET

136
Q

MEN 1 (inheritance)

A

caused by a mutation of menin, a tumor suppressor located on chromosome 11.

137
Q

pituitary adenomas (most commonly a prolactinoma), pancreatic endocrine tumors (eg, gastrinoma, insulinoma), and parathyroid adenomas.

A

MEN1

138
Q

Cardiac rhabdomyomas,hamartomas in the central nervous system and skin, mitral regurgitation, ash-leaf spots, cardiac rhabdomyomas, intellectual disability, adenoma sebaceum, renal angiomyolipomas, and seizures.

A

tuberous sclerosis
HAD
chromosome 16.

139
Q

bilateral schwannomas, juvenile cataracts, meningiomas, and ependymomas.

A

Neurofibromatosis type 2 (NF2)

140
Q

Neurofibromatosis type 2 (NF2) (inheritance)

A

autosomal dominant mutation in the NF2 tumor suppressor gene on chromosome 22.

141
Q

Port-wine stain of the face
Leptomeningeal angiomas –> seizures and epilepsy
Intellectual disability
Episcleral hemangiomas –> early-onset glaucoma

A

Sturge-Weber syndrome

142
Q

Sturge-Weber syndrome -> Cause

A

Congenital, noninherited (sporadic) activating mutation in one copy of the GNAQ gene causes an anomaly of neural crest derivatives

143
Q

NF1

A 
Cafe-au-lait spots
Cutaneous neurofibromas
Optic gliomas
Pheochromocytomas
Lisch nodules (pigmented iris hamartomas)
144
Q

Autosomal dominant mutation of the NF1 tumor suppressor gene on chromosome 17
This mutation has 100% penetrance

A

NF1

145
Q

Caused by a gain of function mutation in FGFR3 on chromosome 4
leads to decreased chondrocyte activity → decreased endochondral ossification → short long bones

A

Achondroplasia

146
Q

Short stature → normal torso; large head; short, plump extremities
Craniofacial changes → prominent brow, recessed midface and nose, middle ear deformities (recurrent otitis media)
Scoliosis, spinal stenosis
Otherwise normal development → normal intellect, normal organ systems, normal endocrine function

A

Achondroplasia

147
Q

X-ray → frontal skull prominence, midface hypoplasia, scoliosis, spinal stenosis
Labs → all endocrine and metabolic labs will be normal
Genetic testing is not frequently required

A

Achondroplasia

148
Q

Mesenchymal cells differentiate into osteoblasts

Osteoblasts form bone directly without a cartilage model

A

Intramembranous

149
Q

Intramembranous -> examples

A

Facial bones
Skull
Clavicle

150
Q

Mesenchymal cells differentiate into chondroblasts
Cartilage matrix forms model in the diaphysis of bones
Osteoblasts develop within the model
Osteoblasts replaced the cartilage model with bone

A

Endochondral

151
Q

Endochondral->examples

A 
Long bones (limbs)
Axial skeleton (vertebrae, ribs)
152
Q

night sweats, insomnia, low-grade fevers, and lymphadenopathy,anorexia and weight loss

A

lymphoma

153
Q

characterized histologically by Reed-Sternberg cells

A

Hodgkin lymphoma->nodular sclerosing type

154
Q

Associated with Epstein-Barr virus ( lymphoma)

A

Hodgkin lymphoma

155
Q

lymphoma with bimodal distribution

A

Hodgkin lymphoma-> Bimodal distribution: young adulthood and
older than 55 years; more common in men except for
nodular sclerosing type

156
Q

Localized, single group of nodes with
contiguous spread (stage is strongest predictor
of prognosis) (lymphoma)

A

Hodgkin lymphoma

157
Q

Better prognosis ( lymphoma)

A

Hodgkin lymphoma

158
Q

May be associated with autoimmune diseases and viral infections (eg, HIV, Epstein-Barr virus, human T-lymphotropic viruses) (Lymphoma)

A

Non-Hodgkin Lymphoma

159
Q

Can occur in children and adults (Lymphoma)

A

Non-Hodgkin Lymphoma

160
Q

Multiple lymph nodes involved; extranodal

involvement common; non-contiguous spread

A

Non-Hodgkin Lymphoma

161
Q

large γ spike, also known as an “M spike via serum protein electrophoresis (SPEP)

A

multiple myeloma

162
Q

MM, there are multiple forms of renal disease. The most common is ->

A

myeloma cast nephropathy.

163
Q

In MM, the acronym CRAB is helpful for remembering the symptoms:

A

hyperCalcemia, Renal failure, Anemia, and Bone pain.

164
Q

Bence-Jones protein

A

abnormal light chain fragment produced by abnormal plasma cells

165
Q

Renal injury->Caused by decreased renal perfusion

A

Pre-Renal Injury

166
Q 
Cardiorenal syndrome
Drugs → NSAIDs
Hepatorenal syndrome
Hypotension
Hypovolemia
Renal artery stenosis
(renal injury->
A

Pre-Renal Injury

167
Q

Caused by direct damage to the kidney (renal injury)

A

*Acute interstitial nephritis
*Drugs (antibiotics, phenytoin, cyclosporine, NSAIDs)
Infections (viral and fungal)
*Acute tubular necrosis-> Ischemia, nephrotoxic drugs, myoglobin, Bence-Jones proteins
*Vascular diseases (HUS, TTP, scleroderma)

168
Q

Caused by urinary obstruction (renal injury)

A

Acquired obstruction-> BPH, iatrogenic, tumors, stones
Congenital obstruction-> posterior urethral valves
Neurogenic bladder-> Diabetes mellitus, opioids

169
Q

most susceptible to Acute Tubular Necrosis

A

Proximal convoluted tubule and thick ascending limb

170
Q

Oliguria < 400 mL of urine/day,Hyperkalemia, metabolic acidosis, uremia
Post qx, hypotension, sepsis → death of tubular cells Granular, muddy brown casts on urinalysis

A

Acute Tubular Necrosis

171
Q

Urine Osmolality (mOsm/kg) > 500
FENA < 1%
Serum BUN:Cr > 20:1

A

Prerenal AKI
*Hypovolemia, hypotension (eg, blood loss, dehydration)
↓ effective circulating volume (eg, heart failure)

172
Q 
Urine Osmolality (mOsm/kg) < 350
Urine Sodium (mEq/L) > 40
Serum BUN:Cr < 15:1
A

Intrarenal

173
Q

Septic shock clinical criteria: (2)

A

1) Persistent hypotension requiring vasopressors to maintain mean arterial pressure ≥ 65 mm Hg, and
2) Lactate ≥ 2 mmol/L

174
Q

principal cytokine mediator involved in septic shock is

A

tumor necrosis factor (TNF)-α -> activates the endothelium and causes WBC recruitment-> extensive systemic vasodilation

175
Q

autoimmune destruction of melanocytes and causes sharply demarcated, asymptomatic macules and patches that are concentrated around body orifices and the hands and wrists

A

Vitiligo

176
Q

confusion, ophthalmoplegia, and ataxia

A

developing thiamine deficiency, and Wernicke-Korsakoff syndrome

177
Q

urinary incontinence, gait ataxia, and cognitive dysfunction.

A

Normal pressure hydrocephalus (NPH

178
Q

Rupture of the middle meningeal artery

A

Epidural Hematoma

179
Q

ucid interval
Rapid expansion → lethargy, coma
Transtentorial herniation → cranial nerve III palsy

A

Epidural Hematoma

180
Q

Imaging -> Biconvex, hyperdense collection of blood

Does not cross suture lines

A

Epidural Hematoma

181
Q

Rupture of Charcot-Bouchard pseudoaneurysms in lenticulostriate vessels

A

Intraparenchymal Hemorrhage

182
Q

Severe, systemic hypertension (typically systolic blood pressure ≥ 180 mm Hg)
Vasculitisc
(Brain hematomas)

A

Intraparenchymal Hemorrhage

183
Q

Imaging->Hyperdense collection of blood in brain tissue

A

Intraparenchymal Hemorrhage

184
Q

Rupture of a saccular aneurysm or arteriovenous malformation

A

Subarachnoid Hemorrhage

185
Q

Autosomal dominant polycystic kidney disease
Coarctation of the aorta
Connective tissue disease

A

Subarachnoid Hemorrhage/risk factors

186
Q

Sudden onset headache
“Worst headache of my life”
Bloody cerebrospinal fluid

A

Subarachnoid Hemorrhage

187
Q

Imaging-> Collection of blood within the cisterns

A

Subarachnoid Hemorrhage

188
Q

Tearing of the bridging veins

A

Subdural Hematoma

189
Q

Subdural Hematoma Risk factors

A 
Alcoholism
Anticoagulation
Cerebral atrophy
Older patients
Falls
190
Q

Acute → confusion, headache

Chronic → cognitive decline

A

Subdural Hematoma

191
Q

Crescent-shaped hemorrhage
Crosses suture lines
Hyperdense (acute) or hypodense (chronic)
Midline shift

A

Subdural Hematoma

192
Q

decreasing renal plasma flow (RPF), increasing glomerular filtration rate (GFR) and increasing the filtration fraction (FF)

A

efferent arteriole.

193
Q

Renal plasma flow can be estimated

A

by para-aminohippurate (PAH)

194
Q

decreased renal plasma flow, increased glomerular filtration rate and increased filtration fraction

A

Afferent arteriole

195
Q

Initial screening tests In cases of suspected Cushing’s syndrome

A

include a 24-hour urinary free cortisol or low-dose dexamethasone suppression test.

196
Q

With an adrenal adenoma, 24-hour urinary free cortisol levels will be

A

elevated, but ACTH levels will be low because these tumors secrete cortisol

197
Q

benign ovarian tumor associated with ascites and a pleural effusion

A

Meigs syndrome-> fibroma of the ovary

  • sex-cord stromal
  • *intersecting bundles of spindle cells with abundant collagen
198
Q

ovary tumor -> nests of urothelium-like cells in a fibrous stroma

A

Brenner tumor

B= Bladder transitional tissue

199
Q

Call-Exner bodies, which are small, round spaces filled with eosinophilic fluid and lined with a ring of cells, which resembles an ovarian follicle.

A

Granulosa cell tumors

200
Q

Papillary serous cystadenocarcinoma of the ovary is notable for

A

psammoma bodies

201
Q

Struma ovarii is a monodermal teratoma with a predominance of

A

thyroid tissue

  • *histologic examination will reveal follicles filled with colloid
  • *symptoms of hyperthyroidism
202
Q

Decreased cerebral blood flow due to vasoconstriction will occur with

A

Alkalosis

203
Q

Hypoventilation will be the appropriate respiratory compensation for

A

Metabolic Alkalosis

204
Q

Left shift in oxygen-hemoglobin dissociation curve will decrease oxygen delivery to tissues and is seen in

A

Alkalosis

205
Q

Papilledema, a sign of acute

A

CO2 retention

**This would create an acid base disorder consistent with respiratory acidosis.

206
Q

neural tube fails to close, leaving a plate-like mass of neural tissue that is

A

Ectodermal origin

207
Q

Endoderm forms the lining of

A

gastrointestinal tract and respiratory system

208
Q

epiblast gives rise to

A

all three germ layers of the embryo: ectoderm, mesoderm, and endoderm

209
Q

hypoblast, or primitive endoderm, gives rise to

A

extraembryonic structures only, such as the lining of the yolk sac.

210
Q

somatopleuric mesoderm makes important contributions

A

skin (dermis) and non-muscle portions of the limbs.

211
Q

splanchnopleuric mesoderm forms

A

heart and the muscles of the gastrointestinal tract and urinary system

212
Q

Ectoderm differentiates to form

A

-the nervous system, tooth enamel, epidermis, lining of the mouth, anus, nostrils, sweat glands, hair and nails.

213
Q

Acromegaly is a disease caused by

A

excess secretion of growth hormone resulting in accelerated growth of organs and peripheral tissue. The leading cause of death in patients with acromegaly is cardiovascular disease.

214
Q

coarse facial features, large hands and feet, organomegaly, and arthralgias due to joint tissue overgrowth. 10-25% of patients will develop diabetes mellitus

A

Acromegaly -> elevated levels of serum insulin growth factor-1 -> excess growth hormone secretion in adults.

215
Q

Reye syndrome-> histology on light microscope

A

microvesicular steatosis

216
Q

Causes of Microvesicular Steatosis-> (4)

A

Reye syndrome
Acute fatty liver of pregnancy
Hepatitis C virus
Tetracyclines

217
Q

Causes of Macrovesicular Steatosis-> (2)

A 
Insulin resistance (metabolic syndrome and obesity)
Alcohol abuse
218
Q

Apoptosis of hepatocytes is a characteristic light microscopy finding of

A

viral hepatitis

219
Q

Confluent centrilobular necrosis is a characteristic finding of hepatotoxicity secondary to

A

acetaminophen overdose

220
Q

Mallory bodies are intracytoplasmic eosinophilic inclusions of damaged keratin filaments and are seen within hepatocytes in patients with

A

alcoholic hepatitis.

221
Q

Macrovesicular steatosis is a histopathologic finding associated with

A

alcohol-induced liver disease and nonalcoholic fatty liver disease, the latter of which is typically seen in patients with insulin resistance (eg, metabolic syndrome)

STEP1 (19 decks)

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