Patho Flashcards
(221 cards)
1
Q
Apolipoprotein C-II deficiency
A
1 (Hyperchylomicronemia)
2
Q
breaks down the triglycerides in chylomicrons and VLDL to form LDL.
A
Apolipoprotein C-II
3
Q
elevated levels of chylomicrons, triglycerides, and cholesterol.
A
1 (Hyperchylomicronemia)
4
Q
Cofactor for lipoprotein lipase
A
Apolipoprotein C-II
5
Q
- Pancreatitis from elevated triglycerides
- Eruptive xanthomas
- No increased risk of atherosclerosis
- Hepatosplenomegaly
A
1 (Hyperchylomicronemia)
6
Q
- Accelerated atherosclerosis
* Achilles tendon xanthomas
A
2 (Hypercholesterolemia)
7
Q
Low-density lipoprotein receptor or apolipoprotein B-100 deficiency
A
2 (Hypercholesterolemia)
8
Q
2 (Hypercholesterolemia)
Cause:
A
Low-density lipoprotein receptor or apolipoprotein B-100 deficiency
9
Q
Accelerated atherosclerosis
Achilles tendon xanthomas
A
2 (Hypercholesterolemia)
10
Q
Premature atherosclerosis
Palmar xanthomas
A
3 (Dysbetalipoproteinemia)
11
Q
3 (Dysbetalipoproteinemia)
Cause:
A
Apolipoprotein E deficiency
12
Q
Clearance of lipoprotein and chylomicron remnants from circulation
A
Apolipoprotein E
13
Q
Mutations are associated with late-onset Alzheimer disease
A
Apolipoprotein E
14
Q
Overproduction of very low–density lipoprotein
A
4 (Hypertriglyceridemia)
15
Q
- Pancreatitis from elevated triglycerides
* Related to insulin resistance
A
4 (Hypertriglyceridemia)
16
Q
Required for the assembly and secretion of chylomicrons
A
B-48
17
Q
Structural protein for high-density lipoprotein
Activation of lecithin acyltransferase
A
A-1
18
Q
Apo E mediates remnant uptake menos del
A
LDL
19
Q
Found only on alpha lipoproteins
A
A-1
20
Q
Binds LDL receptor
Solo esta en particulas que se originan del intestino
A
B-100
21
Q
Arterial bleeding between skull and dura
A
no cruza la linea media
da “periodo lucido”
22
Q
Ruptura de un aneurisma
A
subarachnoid hemorrhage (SAH)
23
Q
Slow bleeding de un bridging cerebral vein
A
between the dura and arachnoid maters
24
Q
disruption of the middle meningeal artery.
between skull and dura
A
epidural hematoma
25
small-vessel vasculitis (2)
- Granulomatosis with polyangitis (also known as Wegener disease)
- Mixed cryoglobulinemia
26
large arteries vasculitis
Takayasu arteritis.
27
Medium-vessel vasculitis
Polyarteritis nodosa
28
chronic sinusitis, otitis media, and/or perforation of the nasal septum in addition to hemoptysis, cough, and/or dyspnea + Hematuria
Granulomatosis with polyangitis (also known as Wegener disease)
29
Type of Renal involvement in Granulomatosis with polyangiitis (Wegener disease)
crescentic glomerulonephritis
| Hematuria
30
Type of ANCA in Granulomatosis with polyangiitis (Wegener disease)
C-ANCA
31
Type of ANCA in Microscopic Polyangitis
p-ANCA
32
Asthma,Recurrent sinusitis,Purpuric skin lesions,,Polyneuropathy, often wrist or foot drop
***Renal involvement is rare!
Eosinophilic Granulomatosis With Polyangitis
| Churg-Strauss syndrome
33
Granulomatous, necrotizing inflammation in small-sized arteries
Eosinophilic Granulomatosis With Polyangitis
| (Churg-Strauss syndrom
34
* Focal necrotizing vasculitis in small-sized arteries
* Necrotizing granulomas in the lung and upper airway
* Necrotizing glomerulonephritis
Granulomatosis With Polyangitis
| Wegener disease
35
LABS in Wegener disease
- C-ANCA
- No eosinophilia
- Red blood cast in urine
36
Necrotizing vasculitis without granulomas
- Microscopic Polyangitis
| - P-ANCA
37
-Adenocarcinoma (eg, lung, ovary)
-Lung cancer
-Breast cancer
-Lymphoma
Paraneoplastic Syndrome:
Dermatomyositis and polymyositis
38
Involved Site: Dermatomyositis and polymyositis
Muscle fibers
39
Dermatomyositis and polymyositis
| Pathophysiology->
Dermatomyositis → perimysial inflammation (CD4+ T cells)
| Polymyositis → endomysial inflammation (CD8+ T cells)
40
Autoimmune → anti–Jo-1, anti–Mi-2, and anti-SRP
Dermatomyositis and polymyositis
41
Symmetric proximal muscle weakness,Normal deep tendon reflexes,Gottron papules, heliotrope violaceus rash)
Dermatomyositis and polymyositis
42
Presynaptic membrane voltage-gated calcium channels
Lambert-Eaton myasthenic syndrome (LEMS)
| *Small-cell lung cancer
43
Autoimmune → anti-calcium channel antibodies
Lambert-Eaton myasthenic syndrome (LEMS)
44
Proximal muscle weakness that improves with use
Autonomic dysfunction
↓ or absent deep tendon reflexes
Lambert-Eaton myasthenic syndrome (LEMS)
45
Myasthenia gravis ass
Thymoma
46
Acetylcholine receptor in postsynaptic membrane
Myasthenia gravis
47
Autoimmune → anti-acetylcholine receptor antibodies
Myasthenia gravis
48
Muscle weakness that worsens with use
Ocular symptoms → ptosis, diplopia
Bulbar symptoms → dysphagia
Myasthenia gravis
49
decreased generation of thrombin at the end of the coagulation cascade
Hemophilia
50
X-linked ↓ factor VIII
Hemophilia A
51
X-linked ↓ factor IX
Hemophilia B
52
key feature suggestive of hemophilia
isolated abnormal aPTT
53
Impaired inactivation of factor V
factor V Leiden disorder
54
prone to the development of deep vein thromboses
factor V Leiden disorder
| ** patients with calf or proximal thigh tenderness
55
von Willibrand disease (vWD)
defective or reduced levels of von Willibrand factor (vWF), which is an extracellular matrix protein that allows platelet adhesion during initiation of primary hemostasis.
56
Vitamin K is required for the synthesis of factors
II, VII, IX, and X and proteins C and S
57
Hereditary Platelet Disorders: (2)
- Bernard-Soulier Syndrome
| - Glanzmann Thrombasthenia
58
```
↓ glycoprotein Ib
↓ platelet-to-von Willibrand factor adhesion
Large platelets
Bleeding time increased
Platelet count normal or decreased
```
Bernard-Soulier Syndrome
59
```
↓ glycoprotein IIb/IIIa
↓ platelet-to-platelet aggregation
↓ platelet plug formation
Shows no platelet clumping
Bleeding time increased
Platelet count normal
```
Glanzmann Thrombasthenia
60
forming very low–density lipoprotein (VLDL)
Apo B-100
61
Cholesterol is synthesized by the liver by:
HMG-CoA reductase
62
Statins MOA
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
63
Most specific for diagnosing hereditary spherocytosis
-Gold-standard is osmotic fragility test
| ↓ mean fluorescence in eosin 5-maleimide binding test
64
Defective ankyrin and/or spectrin → RBC cytoskeleton defects
hereditary spherocytosis
65
Treatment -> hereditary spherocytosis
Splenectomy
66
Complications-> hereditary spherocytosis
Aplastic crisis with parvovirus B19
67
peripheral blood smear findings in hereditary spherocytosis
On peripheral blood smear, spherocytes and/or Howell-Jolly bodies may be seen.
68
Test reveal an absence of CD55 and CD59
Paroxysmal nocturnal hemoglobinuria (PNH)
69
hemolytic anemia, pancytopenia, and large vein thrombosis (often in the hepatic vein)
Paroxysmal nocturnal hemoglobinuria (PNH)
| **may complain of dark urine in the morning.
70
binds to free hemoglobin and, therefore, will be decreased in patients with hemolytic anemia
Haptoglobin
71
presence of hemoglobin A2 levels > 3.5%
β-thalassemia minor
| ** microcytic anemia (mean corpuscular volume < 80 μm3)
72
Seen in patients post splenectomy or in patients with splenic dysfunction (eg, sickle-cell disease,asplenia,hyposlenia hereditary spherocytosis)
Howell-Jolly bodies
73
Seen in patients with macrocytic, megaloblastic anemia secondary to folate deficiency, vitamin B12 deficiency, or orotic aciduria.
Hypersegmented neutrophils
74
increased RDW is seen in patients with
hereditary spherocytosis, iron deficiency anemia, and macrocytic anemia secondary to folate and vitamin B12 deficiency.
75
Note that spherocytes (and microspherocytes) may also be seen in patients with
- autoimmune hemolytic anemia
- glucose-6-phosphate dehydrogenase deficiency
- Hereditary spherocytosis
76
Chronic Lymphocytic Leukemia Typically affects
older patients
77
peripheral smear will show numerous “smudge” cells
Chronic Lymphocytic Leukemia
78
Chronic leukemias C/Fx
-Inicio insidioso (fatiga > 5 meses) + palpable lymph nodes+ Normocytic anemia and thrombocytopenia.
79
Auer rods are found in the cytoplasm of myeloblasts
acute myelogenous leukemia
| **most notably acute promyelocytic leukemia (APL)
80
APL often develops in
young to middle-aged
| **sudden bleeding gums and multiple ecchymoses
81
acute promyelocytic leukemia (APL) commonly associated with the translocation of chromosome
t(15;17)
82
APL often associated with
disseminated intravascular coagulation
83
Leukemic cells with hair-like projections describe
hairy cell leukemia
| uncommon B cell leukemia.
84
commonly older males with MASSIVE splenomegaly and who have pancytopenia (NO Leukocitosis)
hairy cell leukemia
85
hairy cells are
tartrate-resistant acid phosphatase positive and also exhibit CD11c and CD103
86
Numerous lymphoblasts on peripheral smear are typically seen with
acute lymphoblastic leukemia (ALL)
| **greater than 20% blasts on the peripheral smear and in the bone marrow
87
ALL usually develops in
children
| **fever without evidence of infection is the most common symptom. Patients can also have bleeding from thrombocytopenia.
88
Pencil cells are characteristic of
iron deficiency anemia
89
Acute Lymphoblastic Leukemia T-Cell can present with:
mediastinal mass: dysphagia, dyspnea, superior vena cava syndrome
90
Chronic Myelogenous Leukemia Translocation
9;22
91
IL-1 Secreted by What Cells
Macrophage
92
Induces fever
Induces adhesion molecule expression in endothelial cells
Induces secretion of other cytokines
IL-1
93
IL-1
Induces fever
Induces adhesion molecule expression in endothelial cells
Induces secretion of other cytokines
94
IL-2 Secreted by What Cells
All T cells
95
Induces differentiation of immature T cells into regulatory, cytotoxic, and helper T cells
IL-2
96
IL-3 Secreted by What Cells
All T cells
97
Induces differentiation and growth of immature bone marrow stem cells
IL-3
98
Induce isotype switching for IgG and IgE production
IL-4
99
IL-5 Secreted by What Cells
T helper type 2 cells
100
IL-4 Secreted by What Cells
T helper type 2 cells
101
Induce isotype switching for IgA production and promote eosinophil differentiation/proliferation
IL-4
102
IL-6 Secreted by What Cells
Macrophage
103
Stimulates production of acute phase reactants
IL-6
104
IL-8 Secreted by What Cells
Macrophage
105
Chemokine for neutrophils
IL 8
106
IL-10 Secreted by What Cells
T helper type 2 cells
107
Attenuates inflammation
Decreases MHC II and Th1 cytokine expression
Inhibits activated macrophages and dendritic cells
IL-10
108
Promotes differentiation of Th1 cells
IL-12
109
IL-12 Secreted by What Cells
Macrophage
110
Induces macrophage activation, inhibits Th2 differentiation
IFN-γ
111
IFN-γ Secreted by What Cells
T helper type 1 cells
112
WBC recruitment and vascular permeability
TNF-α
113
TNF-α Secreted by What Cells
WBC recruitment and vascular permeability
114
has a role inhibiting leukotriene production
prostaglandin E2
115
aspirin-exacerbated respiratory disease (AERD)
| MOA
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
acute phase reactants stimulated by IL-6 include:
_Ferritin
- C reactive protein
- Serum Amyloid A
- Fibrinogen
- Cerulosplasmin
117
Activates macrophages and plays an important role in granuloma formation.
IFN-γ
118
Conditions That Cause eosinophilia->
Immunologic disorders
(3)
- Job syndrome (Hyper-IgE Syndrome)
- Idiopathic hypereosinophilic syndrome
- Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
119
Conditions That Cause Eosinophilia -> Allergic Disorders
```
Asthma
Allergic rhinitis
Atopic dermatitis
Drug Rash with Eosinophilia and Systemic Symptoms syndrome
Acute interstitial nephritis
```
120
Conditions That Cause Eosinophilia-> Infectious Disease
- Helminths
- Chlamydial pneumonia
- Allergic bronchopulmonary aspergillosis
121
medications that should be given to patients that present with signs of labor prior to 37 weeks' gestation.
- Bethamethasona ->stimulate surfactant production
| - Tocolytics -> terbutaline (b2 agonist)
122
Consequences of Renal Failure
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
Skin findings -> Sarcoidosis
lupus pernio, a purple discoloration of the nose and cheeks
124
Increased Anion Gap Metabolic Acidosis
```
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or isoniazid
Lactic acidosis
Ethylene glycol
Salicylates (late)
```
125
Normal Anion Gap Metabolic Acidosis
HARDASS
```
Hyperalimentation or hyperchloremia
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
```
126
Commonly tested causes of lactic acidosis include:
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
postictal lactic acidosis. Tonic-clonic seizures
increased anion gap metabolic acidosis-> skeletal muscle hypoxia
128
Formula Anion GAP
Anion gap = Na+ - [Cl- + HCO3-]
| normal anion gap is 8-12 mEq/L
129
Type 1 RTA
characterized by insufficient production of new bicarbonate
130
type 2 RTA
characterized by defective bicarbonate reabsorption in the proximal convoluted tubule (PCT) and increased excretion of bicarbonate in the urine.
131
VHL disease (inherance)
HAD
| VHL gene on chromosome 3
132
Tumors seen with VHL disease include:
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
marfanoid body habitus, mucosal neuromas, medullary thyroid carcinoma, and pheochromocytoma
MEN2B
134
parathyroid hyperplasia, medullary thyroid carcinoma, and pheochromocytomas
MEN2A
135
Both MEN2A and MEN2B are caused by mutations
RET
136
MEN 1 (inheritance)
caused by a mutation of menin, a tumor suppressor located on chromosome 11.
137
pituitary adenomas (most commonly a prolactinoma), pancreatic endocrine tumors (eg, gastrinoma, insulinoma), and parathyroid adenomas.
MEN1
138
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.
tuberous sclerosis
HAD
chromosome 16.
139
bilateral schwannomas, juvenile cataracts, meningiomas, and ependymomas.
Neurofibromatosis type 2 (NF2)
140
Neurofibromatosis type 2 (NF2) (inheritance)
autosomal dominant mutation in the NF2 tumor suppressor gene on chromosome 22.
141
Port-wine stain of the face
Leptomeningeal angiomas --> seizures and epilepsy
Intellectual disability
Episcleral hemangiomas --> early-onset glaucoma
Sturge-Weber syndrome
142
Sturge-Weber syndrome -> Cause
Congenital, noninherited (sporadic) activating mutation in one copy of the GNAQ gene causes an anomaly of neural crest derivatives
143
NF1
```
Cafe-au-lait spots
Cutaneous neurofibromas
Optic gliomas
Pheochromocytomas
Lisch nodules (pigmented iris hamartomas)
```
144
Autosomal dominant mutation of the NF1 tumor suppressor gene on chromosome 17
This mutation has 100% penetrance
NF1
145
Caused by a gain of function mutation in FGFR3 on chromosome 4
leads to decreased chondrocyte activity → decreased endochondral ossification → short long bones
Achondroplasia
146
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
Achondroplasia
147
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
Achondroplasia
148
Mesenchymal cells differentiate into osteoblasts
| Osteoblasts form bone directly without a cartilage model
Intramembranous
149
Intramembranous -> examples
Facial bones
Skull
Clavicle
150
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
Endochondral
151
Endochondral->examples
```
Long bones (limbs)
Axial skeleton (vertebrae, ribs)
```
152
night sweats, insomnia, low-grade fevers, and lymphadenopathy,anorexia and weight loss
lymphoma
153
characterized histologically by Reed-Sternberg cells
Hodgkin lymphoma->nodular sclerosing type
154
Associated with Epstein-Barr virus ( lymphoma)
Hodgkin lymphoma
155
lymphoma with bimodal distribution
Hodgkin lymphoma-> Bimodal distribution: young adulthood and
older than 55 years; more common in men except for
nodular sclerosing type
156
Localized, single group of nodes with
contiguous spread (stage is strongest predictor
of prognosis) (lymphoma)
Hodgkin lymphoma
157
Better prognosis ( lymphoma)
Hodgkin lymphoma
158
May be associated with autoimmune diseases and viral infections (eg, HIV, Epstein-Barr virus, human T-lymphotropic viruses) (Lymphoma)
Non-Hodgkin Lymphoma
159
Can occur in children and adults (Lymphoma)
Non-Hodgkin Lymphoma
160
Multiple lymph nodes involved; extranodal
| involvement common; non-contiguous spread
Non-Hodgkin Lymphoma
161
large γ spike, also known as an “M spike via serum protein electrophoresis (SPEP)
multiple myeloma
162
MM, there are multiple forms of renal disease. The most common is ->
myeloma cast nephropathy.
163
In MM, the acronym CRAB is helpful for remembering the symptoms:
hyperCalcemia, Renal failure, Anemia, and Bone pain.
164
Bence-Jones protein
abnormal light chain fragment produced by abnormal plasma cells
165
Renal injury->Caused by decreased renal perfusion
Pre-Renal Injury
166
```
Cardiorenal syndrome
Drugs → NSAIDs
Hepatorenal syndrome
Hypotension
Hypovolemia
Renal artery stenosis
(renal injury->
```
Pre-Renal Injury
167
Caused by direct damage to the kidney (renal injury)
*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
Caused by urinary obstruction (renal injury)
Acquired obstruction-> BPH, iatrogenic, tumors, stones
Congenital obstruction-> posterior urethral valves
Neurogenic bladder-> Diabetes mellitus, opioids
169
most susceptible to Acute Tubular Necrosis
Proximal convoluted tubule and thick ascending limb
170
Oliguria < 400 mL of urine/day,Hyperkalemia, metabolic acidosis, uremia
Post qx, hypotension, sepsis → death of tubular cells Granular, muddy brown casts on urinalysis
Acute Tubular Necrosis
171
Urine Osmolality (mOsm/kg) > 500
FENA < 1%
Serum BUN:Cr > 20:1
Prerenal AKI
*Hypovolemia, hypotension (eg, blood loss, dehydration)
↓ effective circulating volume (eg, heart failure)
172
```
Urine Osmolality (mOsm/kg) < 350
Urine Sodium (mEq/L) > 40
Serum BUN:Cr < 15:1
```
Intrarenal
173
Septic shock clinical criteria: (2)
1) Persistent hypotension requiring vasopressors to maintain mean arterial pressure ≥ 65 mm Hg, and
2) Lactate ≥ 2 mmol/L
174
principal cytokine mediator involved in septic shock is
tumor necrosis factor (TNF)-α -> activates the endothelium and causes WBC recruitment-> extensive systemic vasodilation
175
autoimmune destruction of melanocytes and causes sharply demarcated, asymptomatic macules and patches that are concentrated around body orifices and the hands and wrists
Vitiligo
176
confusion, ophthalmoplegia, and ataxia
developing thiamine deficiency, and Wernicke-Korsakoff syndrome
177
urinary incontinence, gait ataxia, and cognitive dysfunction.
Normal pressure hydrocephalus (NPH
178
Rupture of the middle meningeal artery
Epidural Hematoma
179
ucid interval
Rapid expansion → lethargy, coma
Transtentorial herniation → cranial nerve III palsy
Epidural Hematoma
180
Imaging -> Biconvex, hyperdense collection of blood
| Does not cross suture lines
Epidural Hematoma
181
Rupture of Charcot-Bouchard pseudoaneurysms in lenticulostriate vessels
Intraparenchymal Hemorrhage
182
Severe, systemic hypertension (typically systolic blood pressure ≥ 180 mm Hg)
Vasculitisc
(Brain hematomas)
Intraparenchymal Hemorrhage
183
Imaging->Hyperdense collection of blood in brain tissue
Intraparenchymal Hemorrhage
184
Rupture of a saccular aneurysm or arteriovenous malformation
Subarachnoid Hemorrhage
185
Autosomal dominant polycystic kidney disease
Coarctation of the aorta
Connective tissue disease
Subarachnoid Hemorrhage/risk factors
186
Sudden onset headache
"Worst headache of my life"
Bloody cerebrospinal fluid
Subarachnoid Hemorrhage
187
Imaging-> Collection of blood within the cisterns
Subarachnoid Hemorrhage
188
Tearing of the bridging veins
Subdural Hematoma
189
Subdural Hematoma Risk factors
```
Alcoholism
Anticoagulation
Cerebral atrophy
Older patients
Falls
```
190
Acute → confusion, headache
| Chronic → cognitive decline
Subdural Hematoma
191
Crescent-shaped hemorrhage
Crosses suture lines
Hyperdense (acute) or hypodense (chronic)
Midline shift
Subdural Hematoma
192
decreasing renal plasma flow (RPF), increasing glomerular filtration rate (GFR) and increasing the filtration fraction (FF)
efferent arteriole.
193
Renal plasma flow can be estimated
by para-aminohippurate (PAH)
194
decreased renal plasma flow, increased glomerular filtration rate and increased filtration fraction
Afferent arteriole
195
Initial screening tests In cases of suspected Cushing’s syndrome
include a 24-hour urinary free cortisol or low-dose dexamethasone suppression test.
196
With an adrenal adenoma, 24-hour urinary free cortisol levels will be
elevated, but ACTH levels will be low because these tumors secrete cortisol
197
benign ovarian tumor associated with ascites and a pleural effusion
Meigs syndrome-> fibroma of the ovary
* sex-cord stromal
* *intersecting bundles of spindle cells with abundant collagen
198
ovary tumor -> nests of urothelium-like cells in a fibrous stroma
Brenner tumor
| B= Bladder transitional tissue
199
Call-Exner bodies, which are small, round spaces filled with eosinophilic fluid and lined with a ring of cells, which resembles an ovarian follicle.
Granulosa cell tumors
200
Papillary serous cystadenocarcinoma of the ovary is notable for
psammoma bodies
201
Struma ovarii is a monodermal teratoma with a predominance of
thyroid tissue
* *histologic examination will reveal follicles filled with colloid
* *symptoms of hyperthyroidism
202
Decreased cerebral blood flow due to vasoconstriction will occur with
Alkalosis
203
Hypoventilation will be the appropriate respiratory compensation for
Metabolic Alkalosis
204
Left shift in oxygen-hemoglobin dissociation curve will decrease oxygen delivery to tissues and is seen in
Alkalosis
205
Papilledema, a sign of acute
CO2 retention
| **This would create an acid base disorder consistent with respiratory acidosis.
206
neural tube fails to close, leaving a plate-like mass of neural tissue that is
Ectodermal origin
207
Endoderm forms the lining of
gastrointestinal tract and respiratory system
208
epiblast gives rise to
all three germ layers of the embryo: ectoderm, mesoderm, and endoderm
209
hypoblast, or primitive endoderm, gives rise to
extraembryonic structures only, such as the lining of the yolk sac.
210
somatopleuric mesoderm makes important contributions
skin (dermis) and non-muscle portions of the limbs.
211
splanchnopleuric mesoderm forms
heart and the muscles of the gastrointestinal tract and urinary system
212
Ectoderm differentiates to form
-the nervous system, tooth enamel, epidermis, lining of the mouth, anus, nostrils, sweat glands, hair and nails.
213
Acromegaly is a disease caused by
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
coarse facial features, large hands and feet, organomegaly, and arthralgias due to joint tissue overgrowth. 10-25% of patients will develop diabetes mellitus
Acromegaly -> elevated levels of serum insulin growth factor-1 -> excess growth hormone secretion in adults.
215
Reye syndrome-> histology on light microscope
microvesicular steatosis
216
Causes of Microvesicular Steatosis-> (4)
Reye syndrome
Acute fatty liver of pregnancy
Hepatitis C virus
Tetracyclines
217
Causes of Macrovesicular Steatosis-> (2)
```
Insulin resistance (metabolic syndrome and obesity)
Alcohol abuse
```
218
Apoptosis of hepatocytes is a characteristic light microscopy finding of
viral hepatitis
219
Confluent centrilobular necrosis is a characteristic finding of hepatotoxicity secondary to
acetaminophen overdose
220
Mallory bodies are intracytoplasmic eosinophilic inclusions of damaged keratin filaments and are seen within hepatocytes in patients with
alcoholic hepatitis.
221
Macrovesicular steatosis is a histopathologic finding associated with
alcohol-induced liver disease and nonalcoholic fatty liver disease, the latter of which is typically seen in patients with insulin resistance (eg, metabolic syndrome)
