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75 Cards in this Set

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List the derivatives of the pharyngeal pouches.
Pharyngeal Pouches:
1: Epithelium of middle air, auditory tube

2: Epithelium of palatine tonsil

3: Thymus, Inferior Parathyroid

4: Superior parathyroid
Scapular Winging:
Nerve and Muscle Affected
Serratus anterior
Long thoracic N
Serratus anterior:
Action
Fixes scapula against posterior chest wall
Deltoid:
Action
Nerve
Flex, extend, abduct arm

Axillary
Rhomboid Major:
Action
Nerve
Dorsal Scapular

Draws scapula medially
Budding cells in esophagus
Candida
Immune defenses against candida:
Roles of each defense
1) Th1 cells--local defense
2) Neutrophils: prevents hematogenous spread (via phagocytosis)
What distinct infections would low complement predispose someone to?
SHiN bacteria bc can't form MAC
Following total ishemia, when do cardiac myocytes cease to contract?

When does irreversible ischemic injury occur?
Within 60 seconds

Irreversible ischemia ~30 minutes after
First-line treatment for HTN
Thiazide diuretics
First-line treatment for HTN s/p MI
beta-blockers
What is the best way to prevent neonatal tetanus?
Vaccinate mom while she's pregnant with tetanus toxoid.

She'll produce IgG Ab's which will be transferred to the baby via the placenta!
Antithyroid Drugs:
MOA
Examples
How do they differ?
AE
Methimazole, PTU:
Prevent oxidation of iodine in thyroid gland (which prevents iodination of tyrosine residues)

PTU decreases peripheral conversion of T4 to T3, has a shorter half-life, and is drug of choice in pregnancy.

MTZ is a TERATOGEN.

AE: AGRANULOCYTOSIS!!!
34 year-old female
h/o Hypercalcemia treated with neck surgery
Bitemporal visual field defects

Diagnosis
Pathophys of Syx
Hypercalcemia treated with neck surgery likely was a parathryoid adenoma (tumor)

Bitemporal visual defects due to pituitary tumor extending above sella tursica and consequently compressing optic chiasm.

Patient with h/o pituitary and hyperparathyroid tumor should be evaluated for pancreatic tumor because of MEN TYPE 1 SYNDROME
Describe the following stages of acute tubular necrosis:
Initiation
Maintenance
Recovery
Initiation:
Ischemic injury to renal tubules secondary to hemorrhage, acute MI, sepsis, surgery, etc.

Maintenance (24-36 hours after inciting event): Dec'd urine output, fluid overload, inc'd Cr/BUN, hyperkalemia

Recovery (1-2 weeks after maintenance staget): Gradual increase in urine output leading to high-volume diuresis. Electrolyte abnlts may include dec'd K, Mg, PO4, and Ca due to slowly recovering tubular function.
Why is it that human influenza viruses can undergo reassortment when exposed to animal viruses?

How does this lead to pandemic?

Which family of viruses does influenza belong to?

What other virus can undergo this reassortment?
Influenza A is an orthomyxovirus and has a segmented genome. Can undergo genetic reassortment with animal orthomyxoviruses which sometimes result in altered viral surface glycoproteins (eg, hemagglutinin). This can lead to pandemic.

Other virus that can do this is Rotavirus because it is also segmented.

Note: Reassortment involves exchange of entire genome segments, a far more dramatic process than point mutations in genetic drift.
This region of the hypothalamus produces oxytocin and ADH.
Supraoptic and Paraventricular nuclei

Note: oxytocin and ADH are then transported to posterior pituitary for release.
This region of the hypothalamus mediates hunger.
Lateral nuclei

If lesion lateral nuclei-->starvation ensues (no hunger)
This region of the hypothalamus mediates sweating and vasodilation.
Anterior nuclei (via PSymp)

If lesion--> hyperthermia
This region of the hypothalamus mediates satiety.
Ventromedial

If lesion-->hyperphagia and obesity
Hepatic encephalopathy:
Pathophys
Treatment
Treatment MOA
Hepatic damage-->dec'd ability to detoxify nitrogenous wastes (carry out Ammonia-->Urea)

Inc'd ammonia results in disorientation

Tx: Lactulose--bacterial action on lactulose results in acidic colonic contents-->converts absorbable ammonia into nonabsorbable ammonium ion (an ammonia trap)
Von Recklinghausen's Disease:
Presentation
AKA Neurofibromatosis type 1

PNS tumor syndrome
Pts develop neurofibromas, optic nerve gliomas, Lisch nodules (pigmented nodules of iris), CAFE AU LAIT SPOTS
Neurofibromatosis II:
Presentation
B/L CN VIII (vesitbulocochlear) Schwannomas, multiple meningiomas
Sturge-Weber Syndrome:
Presentation
Cutaneous facial angiomas and leptomeningeal angiomas

Skin involvement overlies ophthalmic (V1) and maxillary (V2) distributions of trigeminal nerve

Also presents with MR, seizures, hemiplegia, TRAM-TRACK radiopacities on skull radiographs
Tuberous Sclerosis:
Presentation
Kidney/liver/pancreatic cysts
CNS cortical and subependymal hamartomas
Oslwer-Weber-Rendu Syndrome:
Presentation
Congenital telangectasias
Ruptures may result in epistaxis (rhinitis w/hayfever), GI bleeds, hematuria

NO CYSTS PRESENT
von Hippel-Lindau Disease:
Presentation
Cappilary hemangioblastomas in retina and/or cerebellum

Congenital cysts and/or neoplasms in kidney, liver, pancreas

INc'd risk RCC (b/l)
Enlarged tongue
Jaundice
Hypotonia
Poor feeding
1 month-old

Diagnosis
Congenital hypothyroidism

Causes severe, irreversible MR if not treated immediately (need T4 for normal brain dev't and myelination during early life)
What are the derivates of the aortic arch?
1st--MAXIMAL; maxillary artery

Second = Stapedial and hyoid aa

Third = C is third letter of alphabet-->Carotid artery

4th--4 limbs!--systemic circuln; on left: aortic arch, on right: proximal right subclavian artery

(there is no 5th)

6th arch: pulmonary aa and (on left only) ductus arteriosus
Branchial arch derivates
1-M's, T's--Mandible, malleus incus, muscles of MASTICATION, mylohyoid

2-S's--Stapes, styloid process, stylohyoid

3-Pharyngeal--stylopharyngeus

4th: cricothyroid
6th: everything in larynx except cricothyroid
Branchial pouch derivatives
1st: middle ear
2nd: palatine tonsil
3rd: INFERIOR PARATHY, THYMUS TOO
4th: SUPERIOR PARATHY

Note 4th ends up being more superior than 3rd!
24-year old female
Infertile
Treated with menotropins following single injection of hCG

Explain drug MOA
Menotropin: acts like FSH and leads to formation of dominant ovarian follicle

hCG causes an LH surge
5 year-old
Bounding pulse over upper left sternum
Continuous murmur

Diagnosis
PDA (CONTINUOUS MURMUR)
When do double-stranded DNA breaks occur?
After exposure to ionizing radiation: X-rays, gamma-rays
Describe the events that occur following UV light damage (and subsequent repair) to skin cells.
UV light causes thymine dimer formation

Excision of dimer and surrounding nucleotides by UV-ENDOnuclease (not exo!!)--this is accomplished by nicking strand at thymine dimer

Signals removal and replacement of DNA by POLYMERASE and LIGASE
Anastrozole:
MOA
Use
Used in malignant breast cancer

Prevents aromatization of Androgens to Estrogen

REMEMBER: Estrogen is the main hormone responsible for the growth and dev't of malignant breast tumors

Aromatase inhibitors suppress estrogen to postmenopausal levels.
HER2/neu receptor type
Tyrosine kinase

(Trastuzumab!)
Congenital deafness due to fetal infection
Rubella
Congenital malformed teeth due to fetal infection
Syphilis
Polyarthritis
Rash that began on face and spread downward
Generalized LAD

Diagnosis
Rubella
Congenital rubella:
Presentation
Sensorineural deafness
Cataracts
Cardiac Malformations (PDA)
Describe how Fructose-2,6-bisphosphate affects glucose breakdown.

What is its effect on alanine metabolism?
Note: Alanine is transaminated to pyruvate during gluconeogenesis!
Describe the Calcium-related events for skeletal muscle contraction.
Upon release from Sarcoplasmic Reticulum, calcium binds to TROPONIN C on thin filaments.

This shifts the position of TROPOMYOSIN exposing MYOSIN BINDING SITE on ACTIN filament.

Lasts only a fraciton of a second before calcium resequestered within SR by Ca2+-ATPase pump
Label
A) Globus Pallidus (part of basal ganglia along w/caudate and putamen)

B) Putamen
C) Internal Capsule
D) Caudate (affected in HD)
E) Amygdala (limbic system)
What is the effect of organophosphate poisoning on muscle activity?
Pathophys of Organophosphate poisoning
Treatment
Organophosphate poisoning irreversibly inhibits cholinesterase.


Inc'd ACh concentration in nicotinic synapses (which are also ACh dependent) leads to muscle fasciculations followed by paralysis.

Atropine will reverse muscarinic symptoms, but has no effect on NICOTINIC receptors.

Use PRALIDOXIME to reverse both muscarinig and nicotinic side effects by restoring cholinesterase from its bond with these substances.
MHC I vs MHC II:
Present on which cells?
What does each present?
MHC I: present on all nucleated cells; present self-antigen, tumor antigen, or cell antigen in response to viral infection

MHC II: APCs only (DC's, macs, B cells)--bacterial organisms, viral particles, freely circulating antigenic material is endocytosed and presented
Describe the process of presenting a bacterial antigen on an APC.
Antigen is phagocytosed and is loaded onto MHC II with ACIDIFIED ENDOSOMES.

MHC II protein-antigen complex is then expressed on cell surface for subsequent interaction with T cells

Failure to acidify lysosomes would lead to deficient expression of MHC II bound to foreign antigen and subsequent lack of interaction b/t APCs and T cells
Which enzymes in glycolysis are unidirectional?

How is this overcome during gluconeogenesis?
Unidirectional:
Hexokinase
PFK
Pyruvate Kinase

Enzymes are bypassed via:
Pyruvate Carboxylase (Pyruvate-->OAA)
(-->Malate to exit mitochondria)
Malate--> OAA
OAA-->Phosphoenolpyruvate via Phosphoenolpyruvate carboxykinase (PEPCK)

Then use Fructose 1,6-bisphosphatase (to bypass PFK)
Glucose-6-phosphatase (to bypass hexokinase)
What metabolic processes provide glucose during fasting?
Between meals: glycogenolysis (until glycogen depleted) and gluconeogenesis

After 12-18 hours of fasting (when glycogen is depleted):
Gluconeogensis (OAA-->Malate-->Phosphoenolpyruvate-->Glucose)
What virus is polycistronic?
What structurally enables this?
What does it require?
Echovirus mRNA is polycystronic (contains multiple genes within sema mRNA transcript) and produces polyprotein product.

For individual viral proteins to be generated, polyprotein product must be cleaved by specific viral protease.

Can do this because it's Single Stranded, Positive Sense, and Non-Segmented.
Carvedilol:
MOA
Use
non-specific blockage of beta-1, beta-2, alpha-1

Use in CHF
Describe how Neisseria meningitidis gains access to the CNS.
First colonized nasopharynx
INvades mucosa to gain access to the bloodstream
Spreads to choroid plexus through blood
Passess BBB
Initiates inflammatory response
C3a:
Effects
Component of complement

C3a, 4a, 5a all trigger histamine release from mast cells, resulting in vasodilation and enhanced vasc perm
C5a:
Effects
Vasodilation, enhanced vasc perm

Recruits and activates NEUTROPHILS
5-HETE:
Effects
Associated enzyme
5-Lipoxygenase

Neutrophil chemotaxis
Leukotriene B4:
Effects
Associated enzyme
5-lipoxygenase

Neutrophil chemotaxis
Luekotriene C4:
Effects
Associated enzyme
Vasoconstriction
Bronchospasm***
Inc'd vasc perm

This is true for LK-C4/D4/E4
Lipoxin A4:
Effects
Associated Enzyme
Vasodilation
INHIBITION of neutrophil chemotaxis
Stimulates monocyte adhesion

Made by 12-lipoxygenase
PGI2:
Effects
Associated Enzyme
COX1,2

PGI2 AKA PROSTACYCLIN
Vasodilation
Inhibition of PLT agg
Thromboxane:
Effects
Associated Enzyme
COX-1,2

Vasoconstriction (CONSTRICT)
Promotes PLT agg (PROMOTES)
What is the laboratory cutoff for polycythemia and how would you classify it?
Diagnose
What is being deposited?
Pathophys
Crescent formation consistent with Rapidly Progressive Glomerulonephritis

Slide shows deposition of fibrin

Crescents consist of proliferated glomerular parietal cells, monocytes, macs that have migrated to Bowman's space. As progresses, fibrin becomes sclerotic.

This is sign of severe renal injury. Usually leads to rapid and irreversible loss of renal function.
Diagnose
What is being deposited?
Pathophys
LInear deposits of C3 and IgG consistent with TYpe 1 Rapidly Progressive GN (i.e., GOODPASTURE SYNDROME)

C4 deposition is NOT found.
Ulceration in which segment of the GI tract is LEAST associated with malignancy?
Duodenum

Usually due to H pylori or NSAIDs
65 year-old male
Progressive weight loss
Jaundice
Anorexia
Palpable gall bladder, non-tender

Diagnosis
Most important environmental risk factor
JAUNDICE AND NONTENDER GALLBLADDER IS PANCREATIC CARCINOMA!!!!!!!!!!!!!!

Biggest environmental risk factor is smoking
When is general anesthesia achieved?
How is potency of anesthetic defined?
General anesthesia achieved when threshold amount of anesthetic accumulates in brain

Potency determined by minimal dose to depress CNS; when brain saturated with anesthetic, partial pressure of gas in brain = partial pressure in other compartments. So use alveolar concentration.

Minimal alveolar concentration is used to measure potency: it refers to concentration of inhaled anesthetic that renders 50% of pts unresponsive to painful stimuli.

Lower MAC-->more potent anesthetic
What properties of anesthetics give it a slow onset of action?
High blood/gas partition means highly soluble in blood-->slow onset

High blood/lipid partition-->high solubility in tissues-->slow onset of action
Episodic HTN
Pheochromocytoma
Vitiligo:
Pathophys
Some sort of autoimmune activity (not really known) leads to COMPLETE LOSS OF EPIDERMAL MELANOCYTES
Wilson's Disease:
Treatment
Penicillamine (Cu chelator)
Lead poisoning:
Treatment
Dimercaprol and EDTA (chelators for lead)
Hemochromatosis:
Chelating Treatment
Deferoxamine (BRONZE DIABETES)
Child suddenly dies
Erythroid precursor cells found in liver and spleen

Diagnosis
Pathophys
Extramedullary hematopoiesis likely caused by severe chronic hemolytic anemia, such as beta-thalassemia
What is the effect of beta-blockers on EKG waveforms? Why?
Beta-blockers slow AV conduction and will increase the PR interval.

Remember:
PR interval is the period of time from beginning of atrial depolarization to the beginning of ventricular depolarization. The longer the PR interval, the longer it takes for an electrical stimulus to travel from the SA node to the ventricles via the AV node, bundle of His, and fascicles.
What EKG abnormality is associated with increased risk for Torsade de pointes?

What drugs cause this abnormality?
Long QT; quinidine, sotalol most frequently associated with long QT