Random Crap Flashcards
McCune Albright Syndrome pt presentation
unilateral cafe-au-lait spots,
polyostotic
fibrous dysplasia (bone is replaced by collagen and fibroblasts),
precocious puberty
Peutz-Jeghars Syndrome pt presentation
Hamartomatous polyps in the colon,
dark-colored macules on the mouth, hands, feet, and genitals
Patau syndrome pt presentation
Chromosome 13 trisomy holoprosencephaly cutis aplasia midline defect cleft palate polydactyly rocker-bottom feet heart and kidney defects (polycystic kidney disease)
Edwards syndrome pt presentation
Chromosome 18 trisomy intellectual disability overlapping fingers clenched fists micrognathia rocker bottom feet
What is oppositional defiant disorder?
pattern of anger and irritability with argumentative, vindictive, and defiant behavior toward authority figures lasting > or equal to 6 months
Everything about Warfarin
Warfarin causes “war” in placenta!!!
Inhibits VKOR, which will inhibit Factors 2,7,9,10, Protein C and S
Used for DVT prophylaxis and for arrhythmia prophylaxis
Can cause skin necrosis
Must measure INR and PT regularly
Parts of the adrenal gland - what do they produce
GFR
Glomerulosa - Mineralcorticoids
Fasciculata - Glucocorticoids
Reticularis - Androgen
Pathogenesis/presentation for Pemphigus Vulgaris and Bullous pemphigoid:
Pemphigus vulgaris: Auto-Ab to desmoglein 1/3 (structural support)
Older adults, potentially fatal. Flacid intraepidermal bullae. Separation of keratinocytes so + Nikolsky sign. Oral mucosa involved.
Reticular pattern around epidermal cells
Bullous Pemphigoid: Auto-Ab to hemidesmosomes (connects keratin in basal cells to underlying basement membrane)
Less severe, also older adults. Fluid filled blisters containing eosinophils. Oral mucosa spared. Nikolsky sign -
Linear pattern at epidermal-dermal jxn
what is another name for 21-hydroxylase mutation
CYP21A2
everything about vinca alkaloids
Vincristine and Vinblastine are microtubule inhibitors
Vincristine adverse effect: “crisps” nerves
Vinblastine adverse effect: causes bone marrow suppression
Taxane drugs
ex. paclitaxel
“taxes stabilizes the economy”
causes microtubules to bind so tightly that the cell can’t divide
trastuzumab
a drug that targets the HER2 receptor
adverse effect: dilated cardiomyopathy “tracy with the big boobs goes to church”
Lynch Syndrome
Mismatch repair is defective
Autosomal dominant mutation of mismatch repair genes MLH1 and MLH2
around 80% progress to colorectal cancer
associated with endometrial, ovarian, and skin cancers
what are the thionamides and what is their MOA
Propylthiouracil (PTU) and methimazole
MOA: blocks TPO, inhibiting the oxidation and organification of iodine which ultimately leads to inhibition of thyroid hormone synthesis
PTU is used in first trimester of pregnancy due to methimazole toxicity wherease methimazole is used in second and third trimester of pregnancy
AE: skin rash, aplastic anemia, hepatotoxicity
metabolic acidosis NAGMA
NAGMA means that the anion gap is 8-12 mEq/L. Cl is high compared to bicarb.
HARDASS H- hyperailmentation/hyperchloremia A- Addison disease (dec. Aldosterone) R- renal tubular acidosis D- diarrhea A- acetazolamide (CA inhibitor in the PCT) S- spironolactone (aldosterone receptor blocker) S- saline infusion
Explain fetal circulation
Oxygenated blood comes from the mom through the Umbilical v. then goes into the placenta. The blood goes through the ductus venosus into the IVC.
The blood enters the RA then goes through the foramen ovale to enter the LA. Blood then goes to LV and into the aorta to go to the body.
Deoxygenated blood from the SVC passes through the RA into RV into pulmonary artery then takes the ductus arteriosus to get into descending aorta!
YAY
where is a PDA heard best
pulmonic valve
Misoprost
MOA: PGE1 analong that inc. production of gastric mucous
clinically used for: prevention of NSAID-induced peptic ulcers and induces labor (ripens cervix)
Adverse effects: diarrhea
where is a PDA heard best
pulmonic valve
Misoprost
MOA: PGE1 analong that inc. production of gastric mucous
clinically used for: prevention of NSAID-induced peptic ulcers and induces labor (ripens cervix)
Adverse effects: diarrhea
Behcet syndrome - presentation
What HLA is it associated with?
Small vessel vasculitis in Turkish/Mediterranean ppl.
Involved w/ HLA-B51. May be precipitated by HSV or Parvo.
Recurrent ulcers + erythema nodosum.
Flares last 1-4 wks.
Mesoderm derivatives
GONADS
G- genitourinary system (ureters, kidneys)
O- other (muscle, bone, connective tissue, serous lining of body cavities, CV system, parenchyma)
N- notochord (nucleus pulposus)
A- adrenal cortex
D- dura mater
S- spleen
HLA-DR3 associations
diabetes mellitus type 1 SLE Graves Hashimoto Addisons
SLE dIEd in the GRAVE bc she ADDed HASH
HLA-DR4 associations
Diabetes mellitus type 1
Addisons
Rheumatoid Arthritis
HLA-DR3 and B8
Graves
Job Syndrom (Hyper IgE)`
Symptoms: A- cold Abscess B- baby teeth C- coarse facies D- derm problems E- hyper IgE F- fractures
timing on separation anxiety
if kid is less than 3-4 years then its normal
otherwise it has to last for at least 4 weeks
What murmurs INCREASE with the standing valsalva maneuver?
MVP (dec LV volume) with earlier midsystolic click
Less blood coming into heart - easier to regurgitate back into LA
HCM - Stiff hard ventricle which means lots of pressure. Small amount of blood will make a lot of sound whereas if a lot of blood is coming into the ventricle - blood will stretch out ventricle and normalize pressure. this is why HCM murmur is decreased with leg raise and squatting.
Azathioprine MOA
Purine analog - inhibits PRPP and inhibits purine synthesis
Volume of Distribution -
Vd = amount of drug in body / plasma drug concentration
Low Vd - intravascular - plasma bound protein
High Vd - all tissues like fat
Etiologies of PAH:
Often idiopathic. Mostly females. can be from inactivating mutation BMPR2 that normally inhibits cell proliferation,
Endothelial dysfxn which inc vasoconstriction.
Drugs (amphetamines, cocaine)
3 drug classes to treat Pulm HTN
Endothelin antagonists (bosentan) PDE-5 inhibitors (sildenafil) Prostacyclin analogs (epoprsotenol, iloprost)
Specific Prostacyclin analog used for Pulm HTN:
MOA:
Side effects
PGI2 (prostacyclin) Epoprostenol, iloprost
MOA: direct vasodilation and inhibits platelet aggregation. Inc cAMP
Side effect: flushing, jaw pain
MOA of Montelukast, Zafirlukast:
What are these drugs especially good for
blocks leukotriene receptors (CysLT1). Specifically blocks LTC4, D4, E4.
Especially good for aspirin and exercise induced asthma
MOA of Zileuton
Adverse Effect
5-lipooxygenase inhibitor. Decrease the conversion of arachidonic acid to leukotrienes.
Inhibits bronchoconstriction!
Hepatotoxicity
Class 1A antiarrhythmic drugs
The drugs: Quinidine, Procainamide, Disopyramide
MOA: moderate Na channel blocker, inc AP duration, inc QT interval
Clinical Use: both atrial and ventricular arrhythmias
Adverse Effect: cinchonism (quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia, and torsades due to increased QT interval
Class 1A antiarrhythmic drugs
The drugs: Quinidine, Procainamide, Disopyramide
MOA: moderate Na channel blocker, inc AP duration, inc QT interval
Clinical Use: both atrial and ventricular arrhythmias
Adverse Effect: cinchonism (quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia, and torsades due to increased QT interval
What is the potency of class 1 antiarrhymics
C>A>B
How to read ECG
- P wave. If present - sinus
- R-R. Rhythym. + rate
- QRS. (< 3 tiny boxes)
- PR interval (< 1 box)
- QT interval (less than 1/2 of the RR)
CYP 450 INHIBITORS
SICKFACES.COM RAG S- sodium valproate I- isoniazid C- cimetidine (H2 blocker) K- ketoconazole (-azoles) F- fluconazole A- acute alcohol C- chloremphenicol E- erythromycin (macrolides) S- sulfonamides C- ciprofloxacin (fluoro) O- omeprazole M- metronidazole
R-ritonavir
A- amiodorone
G- grapefruit
Bismuth, sucralfate MOA and what it is used for
Bismuth binds to the base of an ulcer and allows for increased mucus production, can use as quadruple therapy for H.pylori
Sucralfate requires an acidic environment so can NOT use with PPI
Macrolides MOA (erythromycin, clindamycin)
Used for atypical pneumonia (legionella, mycoplasma, chlamydia) Adverse Effects: MACRO M- motility problems A- arrythmias, QT prolongation C- cholestatic hepatitis R- rash O-eosinophilia
Drugs that cause increased SIADH
cyclophosphamide
carbamazapine
SSRIs
Cyclophosphamide uses
MOA
Adverse Effects
blood cancers and solid tumors, nephritic/nephrotic stuff
MOA; DNA alkylating agent
AE: hemorrhagic cystitis (prevent with MESNA), bladder transitional carcinoma
What is Wolff-Parkinson White Syndrome + treatment
MC pre-excitation ventricular arrythmia
There is an extra bundle of Kent
AV node is bypassed
Delta wave is present–> widened QRS and tiny PR interval
treatment: procainamide
Class IB antiarrhythimcs:
MOA:
Used for:
Lidocaine, Phenytoin, Mexiletine
Na blockade
especially ischemic tissue - binds to partially depolarized cardiac tissue
How do the pulmonary arteries travel relative to the main bronchi
RALS
Right artery is ANTERIOR to the right main bronchus
Left artery is SUPERIOR to the left main bronchus
Triad of Rubella
“eye stuff” (cataracts), “ear stuff” (deafness), and “heart stuff” (PDA)
also can see blueberry muffin rash
Central Venous Catheters should be placed at what location(s) to decrease the risk of infection?
Subclavian V. or
Internal Jugular V.
What is the afferent limb of the cough reflex?
the internal laryngeal n. (travels through the piriform recess)
the internal laryngeal n. is a branch of the superior laryngeal n. which is a part of the vagus nerve
What gene is mutated in Fragile X? And how is it mutated?
FMR1 through methylation, which inactivates FMR1 and inhibits transcription
What are the structures in the retroperitoneum?
SADPUCKER S- (suprarenal) adrenal glands A- abdominal aorta & IVC D- duodenum (except 1st part) P- pancreas (only head and body) U- ureters C- colon (only ascending and descending) K- kidneys E- esophagus R- rectum (mid-distal)
What is the function of the cricothyroid m.?
what is it innervated by?
what pharyngeal arch is the cricothyroid m. from?
what other muscles are derived from this pharyngeal arch?
helps with vocalization
external branch of superior laryngeal n.
ONLY the 4th arch
pharyngeal constrictors and levator veli palitini
what is the function of the internal laryngeal n.?
mainly sensory, supplies to vocal folds
what muscles are supplied by the recurrent laryngeal nerve?
what pharyngeal arch are these muscles from?
what sensory function is carried out by the recurrent laryngeal n.?
ALL intrinsic muscles of the larynx EXCEPT cricothyroid m.
6th arch
sensory function below the vocal folds
what nerve is deep to the piriform recess?
internal laryngeal n.
function of IL-3
stimulates growth and differentiation of stem cells in the bone marrow
what is the most important cytokine that is released in the setting of sepsis?
TNF-alpha, activated macrophages stimulate TNF-alpha to induce systemic inflammation via recruitment of additional leukocytes and increasing pro-inflammatory cytokine production (ex. IL-1 and IL-6)
what is lipoxin?
lipoxin A and B are anti-inflammatory mediators that come from lipoxygenase
__________ are a special type of dendritic cells that contain intracytoplasmic granules having the shape of a tennis racquet
Langerhans cells
the tennis racquet granules are called Birbeck granules
What and where are Meissner corpuscles
location: glabrous (hairless) skin
used for light touch, low-frequency vibration
What and where are Pacinian corpuscles
location: deep skin layers, ligaments, joints
used for high-frequency vibration, skin indentation
What and where are Merkel discs
location: finger tips, superficial skin
used for pressure, deep static touch (shapes, edges)
rare: Merkel cell carcinoma, highly malignant
What and where are Ruffini corpuscles
location: finger tips, joints
used for stretch and joint angle changes
Ehrlichia chaffeensis stuff
harbored by white-tail deer in the US; transmitted to humans via tick bite.
spreads to tissue that’s rich in mononuclear cells (bone marrow, lymph nodes, liver, spleen)
peripheral blood: MORULAE (intraleukocytic inclusions) that are mulberry-shaped
alpha-synuclein production in Parkinsons drive what kind of problems?
NON-MOTOR problems (autonomic dysfunction- constipation, vascular sympathetic nerves- orthostatic hypotension)
because the motor problems (bradykinesia, cogweel rigidity, shuffling gate etc.) is driven by the loss of dopamine
How do you differentiate between primary polydipsia and central DI
Primary polydipsia is more psychological than pathological as the pt is simply consuming a lot of water.
In primary polydipsia and DI the urine osmolality is dilute.
Normal person - If a water deprivation test is done, this kicks in ADH activity. This should cause the serum osmolality to increase until it plateaus because all of the ADH receptors in the kidneys have been used. If exogenous vasopressin is then administered the graph should remain plateaued because all of the ADH receptors are used, it doesn’t matter that you’ve given them more ADH.
Primary polydipsia essentially looks exactly like a normal person except for the fact that initially their serum sodium levels will be lower than a normal person.
If it was central DI, and a water deprivation test was done then the urine osmolality would increase slightly but not significantly because there is no ADH. So exogenous vasopressin administration would then cause a huge increase in urine osmolality.
how do you calculate relative risk?
What do the values of relative risk mean?
How is RR strengthened by p-value and confidence interval (CI)
relative risk is calculated usually in a cohort study.
Ex. risk of people who have breast cancer due to daily alcohol consumption.
to calculate: add all the people in the risk of an outcome(ex. breast cancer) to the exposure(ex. alcohol use) and divide that by the people in the risk of that same outcome without the exposure
If RR= 1 (null value), there is no association
If RR >1, exposure is associated with increased disease occurrence
If RR<1, exposure is associated with decreased disease occurrence
RR values are strengthened if the risk due to chance/probability is proven to be low.
If there is a 95% CI and that interval does NOT include the null value (always 1.0), then this automatically means that the p-value will be <0.05. This means that the RR is statistically significant.
Page 260 in FA
what is rales?
popping sound in alveoli due to heart failure
Explain linkage equilibrium and what happens in disequilibrium?
In a normal population: linkage equilibrium means that there is physical distance between two alleles so the chances of them being inherited together is smaller
Linkage disequilibrium: tendency for certain alleles at 2 linked loci to occur together more or less often than expected by chance. Measured in a population, not in a family, and often varies in different populations.
how to calculate the haplotype frequency of the alleles being linked: (frequency of first allele) x (frequency of second allele)
If this calculated value is lower than the frequency of both alleles being inherited together (what they will give in the question), then the population is said to be in Linkage Disequilibrium
what is pleiotropy?
the occurrence of multiple phenotypic manifestations, often in different organ systems, which result from a mutation in a single gene
What is the function of Apo B48
essential because B48 is placed onto chylomicrons; this is the only way chylomicrons can be secreted from the enterocyte
What is the function of Apo B48
essential because B48 is placed onto chylomicrons; this is the only way chylomicrons can be secreted from the enterocyte
MOA of statins
inhibit HMG CoA Reductase
what are the layers of the heart from inside to out?
which layer is most susceptible to ischemic injury?
endocardium myocardium epicardium (visceral layer of serous pericardium) pericardial cavity parietal layer of serous pericardium fibrous pericardium
myocardium (wall pressures are the highest); area with the least amount of blood flow from coronary arteries during systole
What are the layers of the skin?
from superficial to base
COME LET'S GET SUN BURNED stratum corneum lucidum granulosum spinosum basale
characteristics of Psoriasis
Activation of T helper cells and proliferation of keratinocytes. Epidermal hyperplasia (acanthosis) produces erythematous plaques, hyperkeratosis and confluent parakeratosis of the stratum corneum producing the scaling.
Can see pinpoint bleeding from dermal papillae exposure when scales are scraped off: Auspitz sign
Parakeratosis: when keratinocytes still have their nucleus in the stratum corneum
what are the 4 reasons that may cause Minimal Change Disease
MCD: most common nephropathy in kids 4 I's primarily IDIOPATHIC recent infection immunization immune stimulus
what occurs during N3 sleep and what waveform is it on EEG
Deepest sleep.
Sleep walking, night terrors, and bedwetting (Wee and Flee in N3)
Delta waves (low freq, high amplitude)
Difference in side effects b/w nonbenzo hypnotics for insomnia and benzos?
Nonbenzos (Zolpidem, Zaleplom, Eszopliclone) dont affect sleep cycle as much as regular benzos
Difference between first and second gen H1 blockers?
Second gen has less sedating effects because of decrease entry in CNS
What are the layers of the skin?
from superficial to base
COME LET'S GET SUN BURNED stratum corneum lucidum granulosum spinosum basale
First Gen H1 blockers:
Second gen H1 blockers:
and their clinical use.
first gen: Diphenhydramine (benadryl), dimenhydrinate, chlorpheniramine, doxylamine
for allergy, motion sickness, vomiting in pregnancy, sleep
second gen: Loratadine, Fexofenadine, desloratadine
“adines” - used for allergy
Why can diphenhydramine be used for Acute Dystonia in Parkinson patients?
H1 blockers have sedation and anti-muscarinic effects which help the muscle spasms and stiffness
(also have a1 antagonism)
Diphenhydramine and Benztropine are both used for acute dystonia
characteristics of Psoriasis
Activation of T helper cells and proliferation of keratinocytes. Epidermal hyperplasia (acanthosis) produces erythematous plaques, hyperkeratosis and confluent parakeratosis of the stratum corneum producing the scaling.
Can see pinpoint bleeding from dermal papillae exposure when scales are scraped off: Auspitz sign
Parakeratosis: when keratinocytes still have their nucleus in the stratum corneum
what are the 4 reasons that may cause Minimal Change Disease
4 I's primarily IDIOPATHIC recent infection immunization immune stimulus
What are the two main substances that get stuck in the brain in Alzheimer’s
beta-amyloid plaques (excess beta amyloid from insoluble fibrils that accumulate into extracellular amyloid plaques)
AND
neurofibrillary tangles (aggregates of hyperphosphorylated tau protein form intracellular tangled clumps)
What is Ziehl neelson stain used for
Acid fast bacteria (Mycobacteria, Nocardia, Cryptosporidium)
drug that treats pubic lice
Permethrin
this drug is also used for scabies, which affects interdigital skin but presents with small papules, pustules, and burrows
Variceal hemorrhaging is a direct consequence of __________________
Which vein connects the portal vein to the esophagus to cause varices?
portal hypertension
left gastric vein
Characteristics of PSGN
PSGN is a nephritic syndrome which means that the basement membrane is fucked up
happens 2-4 weeks after a Group A Strep Infection in kids and in adults can also be caused by Staph
LM- hypercellular glomeruli
IF- granular (starry sky) appearance due to IgG, IgM, and C3 deposition along GBM and mesangium
EM- subepithelial IC humps
Acute Kidney Injury is common and therefore leads to fluid and salt retention resulting in edema and hypertension
why are vasodilators (arteriolar/venous) not good for long-term therapy of HTN
vasodilators reduce systemic vascular resistance. Baroreceptors can sense this and cause reflex sympathetic activation:
inc. heart rate, cardiac output, contractility AND
RAAS is activated causing sodium and fluid retention
How do you calculate positive predictive value (PPV)?
calculated as the proportion of subjects who truly have the disease among all those with a positive test result`
Antitumor antibiotics (3 classes) and more or less what they do + major side effect
Bleomycin - radical formation - skin hyperpigmentation, pulm fibrosis
Actinomycin D - intercalates into DNA - myelosuppression
Anthracyclines (Doxorubicin, Daunorubicin) - does both of the above mechanisms - DILATED CARDIOMYOPATHY (prevent with dexrazoxane), alopecia
Biggest adverse effect of dihydropyridines
peripheral edema
Ca2+ channel blocking occurs precapillary, so arteriolar dilation, this allows for increased blood flow which then increases capillary hydrostatic pressure and fluid extravasation into interstitium
MOA and clinical use of Flutamide and Bicalutamide
nonsteroidal competitive inhibitors at androgen receptor (decreases steroid synthesis)
use: prostate cancer
MOA and clinical use of Danazol
synthetic androgen that acts as partial agonist at androgen receptors.
use: endometriosis, hereditary angioedema (the drug increases the amount of C1 esterase inhibitor)
MOA and clinical use of Finasteride
5alpha-reductase inhibitor; decreases the amounts of DHT
use: BPH and male-pattern baldness
Polymyositis/Dermatomyositis - similarities and differences
Both: +ANA, inc CK, +anti-Jo, +antiSRP, +anti-Mi-2(helicase)
Poly: Symmetrical shoulder weakness with ENDOmysial inflammation. CD8
Dermatomyositis: also has gottrons papules, heliotrope rash, “shawl and face rash”. CD4. PERImysial and atrophy. For dermatomyositis look for occult malignancy
Explain what happens after PDA is closed/ligated
there is decreased LA pressure–> decreased LV preload
and there is also an increase in LV afterload, this is because before, blood used to enter the aorta and then immediately be shunted to the pulmonary artery.
Now, blood is flowing through the aorta to the rest of the system, so there will be an increase in BP and therefore an increase in LV afterload
MCC of subarachnoid hemorrhage?
MCC of subdural hematoma?
MCC of epidural hematoma?
anterior communicating artery aneurysm that bursts
hemorrhage of bridging veins
tearing of the middle meningeal artery
What is the problem in Open angle glaucoma?
decreased outflow of aqueous humor or increased production
(from uveitis ,RBCs, retinal detachment) all can cause blockages
Medications used to treat open angle glaucoma:
To increase trabecular outflow: (cholinomimetics) Muscarinic agonist
Pilocarpine and Carbachol. both target M3 to contract ciliary muscle leading to pupil constriction. (dec pressure)
To increase uveoscleral outflow: Prostaglandins
Bimatoprost, Latanoprost. inc. outflow of humor via dec. resistance
Side effect: darkens color of iris, eyelash growth
To DEC. Aqueous humor inflow (Production)
Beta (2) blockers: Timolol, betaxolol, carteolol
Alpha agonist: Epinephrine (a1)(works via vasoconstriction of ciliary body), Brimonidine (a2)
Diuretics: Acetazolamide via inhibition of carbonic anhydrase
what is pulmonary alveolar proteinosis?
progressive respiratory dysfunction due to the accumulation of surfactant debris within alveolar spaces.
surfactant is a lipoproteinaceous material that appears pink with PAS staining. It forms lamellar bodies seen on electron microscopy.
debris isn’t being removed because there is impaired alveolar macrophage function.
tx: inhaled GM-CSF replacement therapy
How is atrophy accomplished?
By ubiquitin-proteosome degradation (autophagy of cell components) and then apoptosis
What is apoptosis mediated by and what does this lead to?
Mediated by CASPASES (activated by many different ways) which then activate proteases and endonucleases
Proteases break down cytoskeleton
Endonucleases break down DNA
what are the 4 chronological events/mechanical complications that can happen after an acute MI
- time frame: acute or within 3-5 days
complication: papillary muscle rupture/dysfunction (usually due to RCA occlusion)
findings: acute Mitral Regurg, leading to severe pulmonary edema - time frame: acute or within 3-5 days
complication: interventricular septum rupture
findings: chest pain, hypotension/cardiogenic shock, there will be inc. O2 saturation in Right Ventricle
3.
time frame: within 5 days or up to 2 weeks
complication: free wall rupture (usually due to LAD occlusion)
findings: slit in the Left Ventricle that can lead to cardiac tamponade and sudden death
previous MIs or LV hypertrophy is PROTECTS against rupture!
4.
time frame: up to several months
complication: left ventricular aneurysm
findings: heart failure, angina, ventricular arrhythmias
Why should you NEVER give monotherapy in active TB
Because the bacteria will develop rapid antibiotic resistance
for example: Isoniazid monotherapy would cause 2 forms of gene mutations by the bacteria
1) the bacteria will decrease the amount of catalase-peroxidase enzymes which is what is needed to convert isoniazid to its active metabolite
or
2) the bacteria will modify the protein binding site for isoniazid
therefore, pair Isoniazid with streptomycin, ethambutol and/or pyrazinamide, basically use the RIPE drugs in combination
Why should you NEVER give monotherapy in active TB
Because the bacteria will develop rapid antibiotic resistance
for example: Isoniazid monotherapy would cause 2 forms of gene mutations by the bacteria
1) the bacteria will decrease the amount of catalase-peroxidase enzymes which is what isoniazid needs to kill the bacteria
or
2) the bacteria will modify the protein binding site for isoniazid
therefore, pair Isoniazid with streptomycin, ethambutol and/or pyrazinamide, basically use the RIPE drugs in combination
What are the 4 R’s of Rifampin
RNA Pol Inhibitor
Ramps up P-450
Red/orange body fluids
Rapid resistance if used alone!
drug that is given to help stop serotonin production in serotonin syndrome
cyproheptadine
fyi serotonin syndrome is AMS, neuromuscular excitation, autonomic hyperactivity
What are distinguishing side effects of taking a beta blocker?
Hypoglycemia(no glycogenolysis)
Bronchospasm (no bronchodil)
Heart block
hypotension (if overdose)
What will digoxin toxicity look like?
Hyperkalemia (blocking K from entering cells), “scooped” or depressed ST segments on ECG
+Hypotension/bradycardia
Besides hypotension and bradycardia, what is a major side effect of intoxication from Ca2+ channel blockers
Hyperglycemia (L type calcium channels are found in the pancreas, and blocking them inhibit release of insulin)
What is Recombination?
when 2 chromosomes exchange information via crossing over. Result is having progeny that have mixed traits from both parent viruses. ex.. developing resistance to a medication that one parent virus didn’t have before but the other parent virus did.
Its like a mom and a dad having a baby. Its a complete mix of genetic information and the baby will possess characteristics of both mom and dad. vs reassortment
What is reassortment?
When viruses with segmented genomes (influenza) exchanges genetic material
Ex. a virus that usually infects animals and a virus that normally infects humans end up infecting a cell in a human. Their RNA segments mix together and form a COMPLETELY new virus w/ both RNA. This can lead to antigenic shift and cause pandemics (Spanish flu)
Its like you, a human, mated with a dragon monster and the baby was a weird monster human that had full segments of RNA from you and the dragon monster.
When do you exclude the patients from a study in which they weren’t compliant to, Intention to treat (ITT) or Per Protocol?
Which way is better to avoid bias?
Per protocol is when you remove patients from a study because they weren’t complaint in taking the drug, etc. Reason why researchers want to do this sometimes is because it doesnt’t reflect the rest of the experiment group who is actually complaint. BUT.. ITT is apparently the more fair and unbiased why to conduct research. This is when you dont exclude anyone and leave them in the group they were in. The idea why is that there was some reason why patients weren’t complaint in the study and this needs to be accounted for.
Where does negative selection occur?
Fetal thymus
What is directive counseling and when should a physician do this?
Directive counseling is when you pretty much tell the patient what they need to do. This happens when there is ONLY 1 medically reasonable treatment option.
Ex. Woman wants to keep pregnancy even though it is found to be an ectopic pregnancy and chance of rupture is high. You as physician have to say No because this fetus is sadly not viable and can kill the mother.
What indicates a normal axis on ECG
Lead I and II positive. (-30 to +90)
What causes prolonged QT and why?
Hypocalcemia (Ca enters in phase 2 of A.P.. if no Ca then depolarization/repolarization are prolonged) Drugs (lots of antiarrythmics) Long QT syndrome Levofloxacin Haldol
Etiology of congenital long QT syndrome and 2 different types:
+ Classic presentation of congenital long QT syndrome:
Inherited mutation due to loss of function mutation of Na and K channels. Prolongs depolarization/repolarization and increases risk for ventricular tachyarrhythmias and sudden cardiac death.
Romano-Ward syndrome - aut. dominant, purely cardiac (no deafness)
Jervell and Lange-Nielson syndrome - aut. rec. sensorineural deafness
Young pt. with recurrent seizures(not seizures, just passing out), w/ family history of Sudden cardiac death
What are the 1st, 2nd, and 3rd degree conduction blocks
First degree AV block: Prolonged PR interval (longer than one big box). Can occur with B-blocker use, Ca channel blocker use, and well-trained athletes
tx: nothing
Second degree AV block:
Type 1 (wenckebach)–> progressive lengthening of PR interval until a beat is dropped (P wave not followed by QRS complex). There will also be a variable R-R interval because of this.
tx: nothing
Type 2–> dropped beats that are not preceded by a change in PR interval
tx: pacemaker
Third degree (complete) AV block:
P waves and QRS complex are completely dissociated. Atria and ventricles beat independently of each other. May be caused by LYME DISEASE.
tx: pacemaker
What comprises the Thayer-Martin Agar usually used in Neisseria
vancomycin, polymyxin (colistin), and nystatin
What is Tropheryma whipplei? What disease does it cause? How does it infect? What is the patient’s presentation?
The patient will usually be a middle-aged man with no history of tobacco or alcohol use. The patient will present with diarrhea, malabsorption, weight loss, arthralgia, and in later stages even present with CNS problems (dementia) and heart problems (endocarditis).
The bacteria causes Whipple disease. Basically the bacteria is engulfed by macrophages and then replicates within macrophages. This impairs antigen presentation. Buildup of infected macrophages blocks lymphatic channels which leads to malabsorption.
There will be foamy macrophages that stain PAS (+).
LOL “PAS the FOAMy WHIPped cream in a CAN”
C-cardiac symptoms
A-arthralgias
N-neurologic symptoms
Explain the relationship between these variables in the kidney: FF (filtration fraction), RPF (renal plasma flow), and GFR (glomerular filtration rate)
FF = GFR/RPF
Filtration fraction refers to the amount of “things” that actually get filtered into the lumen from the plasma.
So, how would efferent constriction affect FF?
first the RPF decreases because if there’s vasoconstriction then less amounts of blood plasma goes to the glomerulus in the first place. Then, there is an increase in GFR because pressure to filter the blood increases due to efferent constriction. So finally with an increase in GFR and decrease in RPF, the FF will increase overall.
