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