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OCE One Liners > Medicine > Flashcards

Medicine Flashcards

1
Q

Where would you like to start?

A

I will meet the patient, review records and referrals, establish a chief complaint and HPI, obtain past medical history, past surgical history, current and former medications, allergies, social history, 10 point review of systems, and assign an ASA classification.

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2
Q

Where would you like to start (orthognathic)

A

I will meet the patient, review records and referrals, establish a chief complaint and HPI, obtain past medical history, past surgical history, current and former medications, allergies, social history, 10 point review of systems, and assign an ASA classification. My HPI would focus on their ability to chew, their perceived speech, and any complaints about their esthetic appearance. I would also ask about changes in their occlusion and goals for any treatment. I would ask about TMJ symptoms including clicking popping and episodes of pain.

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3
Q

Where would you like to start (TMJ)?

A

I will meet the patient, review records and referrals, establish a chief complaint and HPI, obtain past medical history, past surgical history, current and former medications, allergies, social history, 10 point review of systems, and assign an ASA classification. I would focus HPI on any history of TMJ dysfunction including clicking, popping, episodes of pain, closed or open lock, and any previous treatments or conservative management they have tried.

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4
Q

Objective assessment

A

I would start with a set of vitals including heart rate, pulse oximetry, blood pressure and temperature, obtain and height and weight and BMI. I would perform a head and neck exam from crown to clavicles using inspection, palpation, and auscultation, an intraoral exam looking at hard and soft tissues, a TMJ exam, airway exam, cranial nerve exam, and cancer screen.

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5
Q

What is hypertension?

A

A pathologic dysregulation of the body’s mechanisms to control blood pressure.
Divided into essential and secondary, staged by systolic blood pressure, and treated with lifestyle modification and pharmacotherapy.

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6
Q

How would you manage blood pressure perioperatively?

A

Defer elective surgery if blood pressure is greater than 180/110.
Continue antihypertensives except ACE inhibitors and diuretics.
Keep intraoperative BP within 20% of baseline.
For hypertensive emergency, activate EMS.

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7
Q

What is angina?

A

Reversible hypoperfusion of the coronary artery system leading to chest pain.
Divided into stable and unstable, depending on whether the pain is relieved by rest.
Stable angina generally means 70% stenotic vessels

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8
Q

What is acute coronary syndrome?

A

Ischemic cardiac disease including unstable angina, NSTEMI (ST depression or T wave inversion), STEMI, or MI.

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9
Q

What is an MI?

A

Myocardial infarction (where muscle dies) secondary to hypoperfusion.

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10
Q

How will you treat ACS?

A

Nitroglycerine 0.3-0.6 mg sublingual, every 5 minutes x3 doses
ASA 325
Oxygen if hypoxic

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11
Q

How does a drug eluting stent work?

A

Slows the rate of neointimal hyperplasia
Sirolimus or paclitaxel
Requires DAPT 12-18 mosw

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12
Q

What are METs?

A

Metabolic equivalents = basal oxygen consumption of a 40 yo, 70kg male
4-6 METs = power walking, 2 flights of stairs

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13
Q

What are complications of doing surgery less than 6 weeks after ACS?

A

Ventricular free wall rupture
Acute mitral regurgitation from papillary muscle necrosis
Interventricular septum rupture

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14
Q

Epinephrine restriction for ACS patients?

A

40 mcg epi (10 mcg/mL = 4cc = 2 carpules)

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15
Q

How long to wait for surgery after DES/BMS placement?

A

6 months

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16
Q

How long to wait for surgery after balloon angioplasty?

A

14 days

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17
Q

How long to wait after MI?

A

6 months - risk of stroke

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18
Q

How do you estimate your patient’s cardiac risk?

A

RCRI - Revised Cardiac Risk Index
Includes - history of ischemic heart disease, CHF, CVD, preop insulin use, Cr>2, and high risk surgery
ONLY estimates cardiac risk!
Alternative is NSQIP but this is less validated.

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19
Q

What is congestive heart failure?

A

Inability of the heart to pump enough blood to meet the metabolic demands of the tissues in the body.
Divided into heart failure with preserved or reduced ejection fraction.
Divided into NYHA class 1-4 by symptoms.
Treated with diuretics and beta blockers.

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20
Q

What is cardiomyopathy?
What are the 4 types?

A

Disease process affecting the muscles of the heart, affecting the ability of the heart to pump or fill.
Diagnosed by echo.
1. Hypertrophic - 2/2 hypertension, thickened walls
2. Hypertrophic obstructive - Genetic, hypertrophy of inter ventricular septum obstructs outflow tract to aorta.
3. Dilated - 2/2 MI, alcoholism
4. Restrictive - infiltration of myocardium. Sarcoidosis, amyloidosis, hemochromatosis.

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21
Q

What is atrial fibrillation?

A

A common arrhythmia caused by abnormal electric foci in the atrium causing an irregularly irregular rhythm. Carries increased risk of stroke, treated with either rate or rhythm control, and typically stroke risk treated with anticoagulation.

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22
Q

How is risk of bleeding/stroke calculated for patients with A fib?

A

CHADS VASC scoring
CHF <40, HTN, Age >75, Diabetes, Stroke, Vascular disease, Age >65, Sex female

HAS BLED - risk of major bleeding in 1 year from AC
HTN
Abnormal renal function
Stroke
Bleeding
Labile INR
Elderly
Drugs/alcohol

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23
Q

What are cardiac considerations for patient s/p heart transplant?

A

Resting HR 90-100
Heart is denervated - no sympathetic or parasympathetic inputs
Does NOT respond to indirect meds like neo, glycol, atropine
Norepi, epi, beta blockers work directly
If there is double P wave on EKG can be 2/2 native atrial tissue left behind

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24
Q

Adjusting sedation/meds for:
Aortic stenosis
Aortic regurg
Mitral stenosis/regurg

A
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25
Q

What are the steps of atherosclerotic plaque accumulation

A

Endothelial cell injury (from HTN)
Macrophage differentiation and lipid uptake to make foam cells
Fatty streak
Smooth muscle migration, fibrous cap
Necrotic core with calcium deposition, cell death, luminal narrowing

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26
Q

What is cor pulmonale?

A

Chronic lung disease can cause right heart strain that eventually becomes dilated or hypertrophic

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27
Q

Describe the renin-angiotensin-aldosterone system

A

Renin is released from the kidney in response to drop in BP or fluid status
Angiotensinogen is released from liver - when Renin interacts, becomes angiotensin I
ACE from the lungs converts angiotensin I –> II
Angiotensin II tells blood vessels to tighten and tells adrenals to release aldosterone
Aldosterone tells kidneys to reuptake Na and water

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28
Q

Describe TACO (transfusion associated circulatory overload) vs TRALI

A

Pulmonary edema developed from volume overload after blood transfusion. Presents with SOB within 6 hours of transfusion, treat with respiratory support, diuretics.

TRALI - SOB during or within 6 hours of transfusion as well. Not related to volume of transfusion, it’s an EXUDATE.

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29
Q

FEV1

A

amount of air expressed in 1 second as a perfentage of the vital capacity
normal is 80%

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30
Q

Obstructive vs restrictive disease

A

Obstructive = decrease in FEV1 as air is obstructed from being forced out of the lungs
Restrictive = decreased lung capacity in general 80%

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31
Q

What is asthma?

A

Asthma is a reactive respiratory disease characterized by chronic obstruction, bronchiolar inflammation, and hyperresponsiveness leading to wheezing and dyspnea.
diagnosed by PFTs (FEV1/FVC less than 80% of normal, improves with albuterol) or by methacholine challenge (muscarinic/cholinergic agonist)

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32
Q

How to treat bronchospasm? status asthmaticus?

A
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33
Q

What is COPD?

A

An irreversible obstructive-pattern lung disease characterized by either chronic bronchitis or emphysema, generally caused by smoking or alpha 1 antitryptase deficiency.
Characterized by wheezing, coughing, hyperinflation of chest.
Chronic bronchitis - increased mucus production causes obstruction
Emphysema - airway destruction in distal bronchioles, loss of elasticity, trapping air

COPD patients live in chronically hypercarbic state, so hypercarbia does not trigger them to breathe anymore, hypoxemia does!

Stage 3/4 (FEV1 is 30-50%) are ASA 4 –> no nitrous, no sedation

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34
Q

What is a PE?

A

Complete or partial blockage of pulmonary arterial vasculature leading to V/Q mismatch. Common sources include lower extremity veins, mural thrombosis from A fib, or a fat embolism from long bone. Characterized by chest pain, dyspnea, hemoptysis, cyanosis, JVD.

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35
Q

What is included in the Well’s criteria for PE?

A

previous PE/DVT
tachycardia
recent surgery/immobilization
*clinical signs of DVT
*alternative diagnosis less likely
hemoptysis
cancer

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36
Q

How to treat PE?

A
  • CT pulmonary angiogram
  • heparin gtt or lovenox 1mg/kg BID
  • if massive/submassive, consider fibrinolytics vs thrombectomy
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37
Q

What is cystic fibrosis?

A

Autosomal recessive disease due to altered chloride and water transport, preventing sodium reabsorption.
Impacts respiratory system with recurrent infections, productive cough. OBSTRUCTIVE pattern.
GI malabsorption, exercise intolerance, infertility.
A/w diabetes, biliary obstruction –> cirrhosis.

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38
Q

Treatment of CF

A

Prophylactic antibiotics, chest PT, dornase alfa to thin secretions. Pancreatic enzyme replacement.
CFTR modulators can improve the function of the malformed protein formed by the F508del gene.

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39
Q

What is COVID-19?

A

SARS-Coronavirus 2 is a single stranded + sense RNA virus
Transmission through direct contact and droplets
Increased susceptibility in patients with HTN, DM, COPD, blacks, males.

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40
Q

How does COVID-19 infect cells?

A

SARS-CoV-2 binds to human ACE2 receptors (prevalent in alveolar epithelial cells) –> immune cell activation in pulmonary vessels –> multiple organ involvement, thrombosis, AKI, cardiomyopathy.

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41
Q

What are some head and neck manifestations of COVID-19?

A

Cutaneous lesions of maculopapular rash, vascular obstruction, hives.
Xerostomia, vesiculobullous lesions, aphthous ulcers, dysgeusia, facial pain

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42
Q

What else is associated with allergic rhinitis and how is it mediated?

A

IgE-mediated - mast cells degranulate
Associated with asthma, sinusitis, sleep disorders, malocclusions that lead to mouth breathing

Non-Allergic Rhinitis w/ Eosinophilia Syndrome = anosmia, chronic sinusitis, ASA intolerance

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43
Q

What is ARDS

A

Acute Respiratory Distress Syndrome is an acute-onset lung injury characterized by poor oxygenation, bilateral pulmonary infiltrates, and acute time course. There is capillary endothelial injury and diffuse alveolar damage. Problem is that due to hypoxemia, patients will have pulmonary artery vasoconstriction.

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44
Q

What is pulmonary hypertension?

A

Mean pulmonary arterial pressure > 20 (normal is 8-20) as measured by right heart cath. Can be idiopathic or hereditary from a mutation in the Block of Muscle PRoliferation gene (BMPR).
Can be secondary to systemic sclerosis, pulm vasoconstriction from cocaine/meth, HIV.
Increased pulmonary art pressure –> smooth muscle proliferation of media/intima –> fibrosis

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45
Q

What is OSA? CSA?

A

Obstructive Sleep Apnea is a sleep disorder characterized by apneas and hypopneas related to upper airway collapse during sleep.
CSA the absence of respiratory effort leading to apnea during sleep.

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46
Q

What is a hypopnea? Apnea? RERA?

A

Apnea - cessation of airflow at the nostrils and mouth for 10+ seconds
Hypopnea - 50% reduction of airflow for 10 sec w/ 3% sat drop OR 30% reduction of airflow for 10 sec with 4% sat reduction
RERA - an event that causes arousal or decrease in saturation without being apnea/hypopnea

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47
Q

What are the stages of sleep?

A

N1 - lightest - slow eyes, low amp EEG
N2 - Sleep Spindles, K Komplexes
N3 - deep sleep, high amp EEG
REM - mixed sawtooth EEG, REM, atonia

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48
Q

What is the pathophysiology of OSA?

A

Increased sympathetic tone
hypoxia followed by oxygenation leads to production of free radicals and endothelial damage, activation of PMNs, release of inflammatory mediators. Chronic inflammatory state.

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49
Q

What is the STOP-BANG questionnaire?

A

Snore?
Tired?
Observed stop breathing?
Pressure (HTN)?

BMI >35
Age >50
Neck >16inches
Gender M

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50
Q

Respiratory considerations for OSA?

A

Lung volumes reduced, decreased FRC and ERV
Ventilation shifted to upper lungs –> worse V/Q mismatch, lower PaO2

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51
Q

What signs concerning for OSA can you see on lateral cephalogram?

A

PAS = B point to gonion - <11 means BOT obstruction
Long soft palate P-PNS >37
Inferiorly positioned hyoid >15 to mandibular plane means UPPP will fail

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52
Q

Extrapulmonary TB and tx

A

Meningitis, Pott’s disease (vertebral), miliary TB, pericarditis, scrofula
RIPE
Rifampin, Isoniazid, Pyrazinamide, Ethambutol (+B6)

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53
Q

How does heparin work? What is difference between hep and LMWH?

A

Heparin binds to and upregulates AntiThrombin-3 which shuts down clotting cascade in multiple places
Heparin - molecules varied in size, bind to other factors –> unpredictable
LMWH - all smaller molecules, mostly only hits Factor Xa - to check, Anti-Xa Assay.
Protamine Sulfate (salmon!!) can reverse hep gtt or 60% of LMWH

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54
Q

Where are clotting factors produced?

A

All are made in the liver except Factor VIII and VWF (made in endothelial cells)

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55
Q

How to reverse warfarin?

A

Prothrombin Complex Concentrate (PCC = Factors 2, 7, 9, 10), Fresh Frozen Plasma (all coag factors, no platelets)

Cryo has VWF, fibrinogen

56
Q

What is Gelfoam?

A

Gelatin Porcine Collagen
Forms a scaffold for a clot

57
Q

What is Avitene?

A

Microfibrillar Bovine Collagen - binds platelets and aggregates

58
Q

What is Surgicel?

A

Oxidized methylcellulose
Attracts platelets, precipitates fibrin
Very acidic
NeurotoxicW

59
Q

What is Collaplug?

A

type 1 bovine cross-linked collagen
stimulates platelet adherence and aggregation

60
Q

What is topical thrombin?

A

Bovine thrombin (activated F2a)
Cleaves fibrinogen –> fibrin to stabilize clot

61
Q

What is Amicar mouthrinse?

A

Aminocaproic acid - antifibrinolytic - clot stabilizer by inhibiting plasmin

62
Q

what is TXA mouthrinse?

A

Tranexamic acid 5% - antifibrinolytic - inhibits plasminogen turning to plasmin, stabilizes clot

63
Q

What is FloSeal?

A

Bovine gelatin matrix, CaCl, plasma-derived human thrombin. Swells and expands to 10-20% of size and forms clot.

64
Q

How do you manage anticoagulation in perioperative period for a patient?

A

For a smaller procedure, 2-3 erupted teeth or less, I feel comfortable following literature that has proven safety of continuing anticoagulation with use of local hemostatic measures. For more invasive procedures, I would discuss holding DOACs (Xa inhibitors -aban and direct thrombin inhibitors -atran) with the patient’s cardiologist for 2 days preoperatively.

65
Q

What is hemophilia?

A

X-linked recessive bleeding disorder, there are types including hemophilia A, B, C (AR). Bleeding results from deficiency in factor VIII, IX, or XI. Results in increased PTT from effect on Intrinsic Pathway of coag cascade.
Classified as mild, moderate, severe based on factor levels (>5%, 1-5%, <1%).

66
Q

How is hemophilia managed?

A

Recombinant Factor 8 or 9 infusion prior to procedures. Goal of achieving 80-100% normal factor levels and maintain at 50% for 1-2 weeks postop.
DDAVP works by causing release of F8 and VWF from endothelial cells.

67
Q

What is von Willebrand Disease?

A

The most common inherited bleeding disorder - AD -characterized by quantitative and/or qualitative deficiency of vWF, which mediates platelet adhesion to other platelets as well as to endothelium. vWF also stabilizes Factor 8.

Type 1 - partial quantitative. Treat with DDAVP 0.3 mcg/kg IV preop. (this works because it’s only quantitative - vWF still works!)
Type 2 - Qualitative deficiency
2a - Absence of multimers
2b - hypercoagulable!! no DDAVP
2m - has MultiMers
2n - No affiNity for F8
Type 3 - total quant deficiency

68
Q

How is VWD managed?

A

DDAVP (do not give to 2b) - must monitor free water intake as this is ADH and may cause hyponatremia

Cryoprecipitate - F8, F9, vWF, fibrinogen, fibronectin. F8 concentrate is rich in vWF.
Humate P = vWF/F8
Amicar

69
Q

What is anti-thrombin 3 deficiency?

A

An inherited deficiency of antithrombin 3 causing thrombophilic state, characterized by recurrent thrombosis. Increased protease activity and fibrin formation.
Type 1 - QUANT
Type 2 - QUAL

70
Q

What is Protein C deficiency?

A

Autosomal Dominant deficiency in protein C - protein C inhibits coagulation by inactivating factors 5, 8.
Type 1 - QUANT
Type 2 - QUAL

71
Q

What is Factor V Leiden?

A

Autosomal dominant mutation of Factor V resulting in resistance of F5 to activated protein C –> prothrombotic state.
Heterozygous - 5-10x risk thrombosis
Homozygous - 50-100x thrombosis risk

72
Q

What is multiple myeloma?

A

A malignancy of plasma cells causing production of monoclonal immunoglobulins. This leads to bony lesions, fractures, and hypercalcemia. This is diagnosed by protein electrophoresis, serum and urine M protein, and immunoglobulin light chains (kappa/lambda).

73
Q

What are some types of microcytic anemia?

A

MCV <80

Iron deficiency
Anemia of chronic disease
Thalassemias
Sideroblastic anemia

74
Q

What are some normocytic anemias?

A

CKD
Anemia of chronic disease
Hemolysis
Blood loss
Bone marrow failure
Multiple myeloma

75
Q

What are some microcytic anemias?

A

B12 and Folate deficiency

B12 deficiency also has neurologic abnormalities
B12 def can be from pernicious anemia - autoimmune destruction of gastric parietal cells –> no intrinsic factor telling you to absorb B12

76
Q

What is sickle cell anemia?

A

An autosomal recessive disorder where a point mutation (valine for glutamic acid in the beta-globing chain of hemoglobin) causes sickling of red blood cells and hemolysis

77
Q

What is the difference in a type and screen vs type and cross?

A

Type and cross includes a type and screen (for ABO/Rh) but also cross matches the patient’s blood with the donor blood for reactivity in cases of high chance of antigenicity

78
Q

What is in fresh frozen plasma?

A

Coagulation factors and fibrinogen

79
Q

What is prothrombin complex concentrate (PCC)?

A

Contains coag factors 2, 7, 9, 10, C, S

80
Q

What is cryoprecipitate?

A

Fibrinogen, factor 8, VWF, factor 13, fibronectin

81
Q

What is hereditary spherocytosis?

A

Autosomal dominant defect in RBC membrane (ankyrin or spectrin) causing loss of parts of the membrane and small, round spherocyte RBCs subject to hemolysis.

Diagnosed by osmotic fragility test. Treat with splenectomy.

82
Q

What are the thalassemias?

A

Autosomal recessive anemias related to abnormal production of globin chains.

Alpha chain - controlled by 4 genes - if 1 or 2 are mutated, NBD. If 4 are mutated, death.

Beta chain -
minor = splicing defect - decreased HbA
major = nonsense mutation - NO HbA

83
Q

What is leukemia?

A

Abnormal production of myeloid or lymphoid cells in an acute or chronic manner - from a blockage of stem cell differentiation.
Myeloid = RBC, PMN, macrophages
Lymphoid = B cells, T cells, NK cells

84
Q

What are some risk factors for diagnosis of AML?

A

Down syndrome, Klinefelter’s syndrome, Patau syndrome, neurofibromatosis

85
Q

What are myelodysplastic syndromes?

A

A group of neoplasms from a clonal disorder of hematopoietic stem cells leading to dysplasia and ineffective hematopoiesis. Can transform into AML.

86
Q

What is G6PD deficiency?

A

Glucose-6-phosphate dehydrogenase deficiency - X linked recessive disorder causing intrinsic hemolytic anemia.
G6PD normally works to create NADPH, which protects RBCs from oxidative stress - when exposed to oxidative stress (some meds, fava beans), RBCs lyse and cause Heinz bodies

87
Q

Describe heparin induced thrombocytopenia

A

There are 2 types - 1, asymptomatic, heparin has a direct effect on platelet formation and platelet count decreases in first 48 hours and then spontaneously corrects
type 2 - immune mediated - heparin binds to PF4 (platelet factor 4), IgG binds to that complex, patient becomes hyper coagulable and risk of death

88
Q

What is DIC?

A

Disseminated intravascular coagulation - disordered consumption coagulopathy leading to both bleeding and clotting episodes.

89
Q

What are the MAHAs?

A

Microangiopathic hemolytic anemias

TTP
HUS
DIC

90
Q

How does creatinine clearance estimate renal function?

A

Creatinine is a byproduct of muscle metabolism that is almost exclusively filtered and excreted, not resorbed - good indicated of renal function.

91
Q

What is an AKI?

A

Sudden and reversible reduction in kidney function, usually accompanied by an increase in creatinine of 0.3 in 48 hours.
BUN/Cr helpful for determining cause - pre renal if BUN/Cr > 20:1

92
Q

What is CKD?

A

Permanent renal insufficiency that develops chronically resulting in damage to the renal system and decreased function.
Staged 1-5 by GFR.
1 >90
2 60-90
3 30-60
4 15-30
5 <15 ESRD

93
Q

What fluid do you give for a resuscitative bolus and why?

A

LR 20cc/kg - more physiologically balanced than NS - less chloride specifically, as resuscitating with NS can lead to non-gap metabolic acidosis

94
Q

What does aldosterone do?

A

Causes Na reabsorption and K secretion in the distal kidney

95
Q

How do you manage hyperkalemia?

A

Symptoms = paresthesias, paralysis, confusion, respiratory failure, dysrhythmias, muscle cramps

Evaluate patient, repeat labs to evaluate hemolysis (CBC), EKG
Treat K>6.5
1. Calcium gluconate 1g IV
2. Bicarb 1 amp IV if acidemic.
3. Albuterol 10mg neb
4. Kayexalate, HD

96
Q

What is anion gap?

A

Compare Na to Cl + Bicarb …. normal gap is 8-12 - meaning Na is 8-12 points higher than Cl + Bicarb

97
Q

What is a high anion gap acidosis?

A

This means that there is something else in the blood, typically an acid, increasing the gap

Lactic acid, methanol, ethylene glycol, DKA

98
Q

What is diabetes mellitus?

A

A metabolic disorder characterized by hyperglycemia, either related to insulin resistance or destruction of beta cells.

Diagnosed by HbA1c > 6.5%, fasting glucose >126, or random glucose >200 w/ symptoms

99
Q

How to manage diabetic medications perioperatively?

A

Half nighttime long acting insulin. If they take in the morning, cut by 25-50%.
No morning short acting insulin. Continue insulin pumps as is.
Hold all oral hypoglycemics for 24h.
Hold SGLT-2 inhibitors (-gliflozin) for 3-4 days preop.
Initially guidelines said to hold IM GLP-1 agonists for 1 week preop, now saying continue as usual but 24h liquid diet preop.

100
Q

How does dextrose affect blood sugar?

A

1g of dextrose raises blood sugar by 5 mg/dL
25g dextrose raises by about 125

101
Q

What is HHS?

A

Hyperglycemic hyperosmolar state

Glucose >600
Polyuria, polydipsia
Dehydration
Blurry vision, polyphagia, N/V
Also with inciting event.

101
Q

What is DKA?

A

Metabolic condition secondary to insulin shortage.
glucose > 250
pH <7.3
Bicarb <15
Ketones in blood or urine

Usually due an inciting event - illness, infection, alcohol.

Mgmt - Rehydrate with LR, start insulin and K+ (pseudohyperkalemia due to no insulin)

102
Q

Describe the hypothalamus-pituitary-thyroid axis

A

TRH made in hypothalamus, tells anterior pituitary to make TSH, tells thyroid to make T3 and T4.
80% made is T4, 20% is T3. T3 is active!!!

103
Q

Most common cause of hyper and hypothyroid

A

Hyperthyroid = Graves disease
Autoantibodies stimulate TSH receptors –> high T3, T4

Treatment for hyperT = PTU, methimazole. PTU prevents peripheral and central conversion of T4 to active T3. Methimazole only works within thyroid gland to prevent thyroid peroxidase from making thyroid hormones.

Hypothyroidism = Hashimoto’s - antithyroid antibodies destroy thyroid.

104
Q

How do you manage a patient taking steroids in the perioperative period?

A

If the hypothalamic-pituitary axis is unlikely to be suppressed (steroids <3 weeks, <10mg prednisone daily), continue steroids.

If likely suppressed, ie prednisone 20mg for >3 weeks, and with Cushingoid appearance, would stress dose. 50mg hydrocortisone preop, 25mg q8h x 3 doses postop.

If unsure, stop steroids for 24h and draw 8am serum cortisol. Less than 5, suppressed. Over 10, good to go.

105
Q

How does insulin work?

A

promotes uptake of glucose into muscle, adipose, and liver tissue.

106
Q

how does metformin work?

A

Metformin is a biguanide - decreases hepatic gluconeogenesis, decreases intestinal glucose absoption

107
Q

how do sulfonylureas work?

A

stimulates beta cells to produce insulin

108
Q

how do thiazolidines work (glitazone)?

A

promote insulin sensitivty in adipose, hepatic, muscle tissue.

109
Q

how do GLP-1 agonists work?

A

OZempic, semaglutide
synthetic peptide of glucagon-like peptide that stimulates insulin secretion, decreases glucagon secretion

110
Q

how does sitagliptin/januvia work?

A

This is a DPP4 inhibitor, prevents inactivation of GLP1 and GIP leading to increased insulin secretion

111
Q

What is a myxedema coma?

A

A state of decompensated hypothyroidism characterized by hypoglycemia, hypercapnia, hypoventilation, hypotension, hypothermia, coma.

tx with IV T4/T3, glucocorticoids, supportive care

112
Q

talk about adrenal gland physiology

A

Corticotropin Releasing Factor (CRF) is released from the hypothalamus, tells pituitary to release ACTH, which manages release of cortisol.
Adrenal cortex makes cortisol (glucocorticoid), aldosterone (mineralocorticoid), and androgens. Adrenal medulla makes epi/NE.

113
Q

What is Cushing syndrome?

A

disease of excessive free plasma glucocorticoids, either endogenous or exogenous.
endogenous is either primary adrenal (ACTH independent) or pituitary/ectopic ACTH production (lung ca, pheos, thyroid cancer)

buffalo hump, truncal obesity, striae, cognitive dysfunction, hyperglycemia, hypertension

dx w/ dexamethasone suppression test

114
Q

What is adrenal insufficiency?

A

primary = AI destruction by Addison’s disease - weakness, anorexia, arthralgia, hypotension, hyponatremia, hyperkalemia

secondary = decrease or loss of glucocorticoid secretion usually due to suppression by steroids

115
Q

What is thyroid storm?

A

An acute, life threatening exacerbation of hyperthyroidism triggered by stress of surgery or illness. patients are induced into a hypermetabolic state caused by excess release of thyroid hormones.

arrhythmias, MI, CHF, hyperthermia, tremors, tachycardia

tx = supportive + Na Iodide (blocks release of stored thyroid hormone), PTU, hydrocortisone (prevents conversion of T4 to T3), propranolol

116
Q

What does PTH do?

A

Regulates calcium homeostasis.
Hypocalcemia –> PTH tells GI system to absorb Ca, renal system to retain Ca, and bone to undergo osteoclastic activity

117
Q

Hyper PTH - primary, secondary

A

Primary - parathyroid adenoma
Secondary - hypocalcemia leading to release of excess PTH

can present as Brown’s tumor, loose teeth, sialolithiasis

118
Q

Hypo PTH causes

A

surgically removed parathyroid glands, radiation, autoimmune destruction
DiGeorge syndrome - hypoplasia/aplasia of parathyroid glands

paresthesias, facial muscle spasms

119
Q

What is SIADH?

A

Syndrome of inappropriate ADH, characterized by excessive free water retention leading to dilutional hyponatremia.

can be from ectopic production of ADH (lung cancer), CNS infection, trauma, drugs

120
Q

What is DI?

A

Diabetes Insipidus - dilute urine and excess free water loss

Central - failure to produce ADH - pituitary adenoma, trauma, ischemia

nephrogenic - insensitivity or resistance of kidney to ADH - usually drug related (lithium)

121
Q

What is obesity? How does BMI correlate?

A

Obesity is an abnormally high amount of adipose tissue compared to lean body mass body weight >20% over ideal body weight.

BMI = kg/height
<18.5 underweight
25-29 overweight
30-34 obesity 1
35-39 obesity 2
>40 extreme obesity

BMI 30-40 ASA 1
BMI >40 ASA 3

122
Q

Pregnancy
CV effects
hypercoagulable
radiation

A

1st trimester - organogenesis weeks 3-14

CV effects of pregnancy - increased CO, HR, SR, blood volume, decreased SVR, FRC

Increased coag factors, increased fibrin, gravid uterus causes endothelial damage –> virchow triad

In first 16 weeks, 0.6 Gy radiation has risk of growth restriction, intellectual delay, etc. <0.05 Gy not teratogenic.
1 panorex = 20 microsieverts = 0.0002 Gy

123
Q

Maternal complications of pregnancy

A

gestational diabetes - maternal insulin resistance
gestational hypertension - >160/110
pre-eclampsia - HTN + proteinuria or other end organ damage after 20 weeks
eclampsia - HTN + proteinuria + seizures –> emergent delivery
HELLP - hemolysis, elevated liver enzymes, low platelets. occurs with pre-E and E, immediate delivery

124
Q

How would you manage a pregnant patient?

A

Attempt to perform procedures in second trimester and use drugs that are ideally class A or B.

125
Q

What is SLE?

A

Systemic lupus erythematosus - an autoimmune disease characterized by chronic inflammation due to an autoantibody production. Higher prevalence in women and POC, symptoms include fever, fatigue, weight gain, arthritis, nephritis, pleuritis, pericarditis, Libman sacks endocarditis, anemia

126
Q

What is RA?

A

Chronic systemic inflammatory disease characterized by symmetric inflammatory polyarthritis and progressive destruction of joints.

Juvenile if present for >6 weeks in <16 yo

127
Q

What is myasthenia gravis?

A

autoimmune disorder affecting postsynaptic neuromuscular transmission of the nicotinic ACH receptor due to production of autoantibodies. Presents with skeletal muscle weakness that IMPROVES WITH REST. Commonly patients have a thymoma.

test - patients improve with anticholinesterase!! pyridostigmine!

usually resistant to succinylcholine. avoid aminoglycosides (Z pack), avoid inhalational anesthetics.

128
Q

what is ehlers danlos syndrome

A

Inherited connective tissue disorder resulting from a defect in synthesis or structure of fibrillar collagen. this leads to changes in skin, tendons, blood vessels.

patients have elastic skin, hypermobility, bleeding tendency, aortic fragility, POTS

129
Q

What is Marfan’s syndrome?

A

Autosomal dominant connective tissue disorder due to a mutation in Fibrillin-1, leading to aortic dilation, mitral regurgitation, hypermobility

130
Q

Duchenne Muscular Dystrophy

A

X-linked recessive mutation in dystrophin gene leading to progressive necrosis of muscle fibers, leading to delayed motor skill development, learning disability. Calf pseudohypertrophy, thigh muscle wasting.

Becker muscular dystrophy - less severe variant

myotonic muscular dystrophy - affects smooth and skeletal muscle, myotonia = difficulty relaxing muscle.

131
Q

Osteoarthritis

A

Progressive articular cartilage deterioration and remodeling of subchondral bone. Weight bearing joints are affected first. Pain worse with function.

cartilage goes through roughening, fibrillation, fissuring, erosion. chondrocytes then release proteolytic enzymes causing more destruction and subchondral cysts.

132
Q

Guillan Barre

A

Guillan Barre is an immune-mediated, acute onset inflammatory demyelinating polyneuropathy

133
Q

What is rheumatic heart disease/rheumatic fever

A

Group A Strep pharyngitis infection as a child can lead to rheumatic fever (abnormal immune response to GAS) –> complication of rheumatic fever is rheumatic heart disease which is inflammation and scarring of the heart valves. most commonly mitral valve.

cross reaction of antibodies to Strep M protein with self-antigens on cardiac proteins - type 2 hypersensitivity

134
Q

Which patients are required to have SBE prophylaxis by the AHA?

A
  1. Prosthetic heart valve
  2. Prior infective endocarditis
  3. Cardiac transplant with valve regurgitation
  4. Congenital heart disease AND:

2g amoxicillin (50mg/kg)
Azithromycin 500mg (15 mg/kg) if allergic

135
Q
A

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