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Antipsychotic Neuroleptics

indications: A.Functional psychosis: schizophrenia, schizoaffective disorders, schizophreniform disorder, brief psychotic disorder, mania, postpartum psychosis, psychosis with depressed mood, and delusional disorders.

First Generation Antipsychotics [FGAs] (Also called conventional, typical, or traditional antipsychotics).

Therapuetic effect: in the mesolimbic pathwayD2 blockade reduces active psychotic features. This may take up to 6 weeks to appear)$.

# Antidopaminergic S/E; 1. In Nigrostriatal tract >>> EPSE (because of the resulting hypercholinergic effect, which manifests in skeletal muscle spasms

- Acute dystonia: appears within days after Rx. Severe painful spasm of neck muscles (torticollis), ocular muscles (oculogyric crisis) muscles of the back (opisthotonus) and tongue protrusion.

Parkinsonism: appears within weeks after treatment, its features: stooped posture, akinesia, muscle rigidity, masked face, and coarse tremor. Treated with anticholinergic drugs (e.g. procyclidine)

Rabbit Syndrome Rapid perioral tremor.

cont Super-sensitivity of dopamine receptors. No specific treatment, the only agreed treatment is to discontinue the antipsychotic drug when the patient’s state allows this.

cont Thus, antidopaminergics induce excessive prolactin secretion, which lead to gynecomastia and amenorrhea. Some gynecologists prescribe dopaminergic medications (e.g. bromocriptine) to reverse amenorrhea in psychotic females, which may aggravate their

# Anticholinergic S/E; dry mouth, constipation, urinary retention, poor erection, blurred vision, and precipitation of closed-angle glaucoma.

Haloperidol (Haldol) 10 mg high potency s-e sezure prolonged qt

SDA - olanzapine (zyprexa), quetiapine (seroquel), clozapine (leponex), risperidone (risperdal), & paliperidone (invega).

Therapeutic effects; More specific for the mesolimbic than nigrostriatal dopamine system >>> less EPSE.

> improve negative symptoms of psychosis: low initiation, lack of motivation, and restricted affect. They improve both positive and negative symptoms of psychosis and can help some resistant cases.

Adverse effects; Less EPSE, antiadrenergic, anticholinergic S/E. but there is a high risk of metabolic syndrome ( see below).

Olanzapin Advantage Effective on negative
features

Clozapin se Agranulocytosis Metabolic syndrome + Agranulocytosis (check WBCs). + High risk of
seizures

Quetiapin se Metabolic syndrome

Third Generation Antipsychotics Dopamine System Stabilizers [DSS].

DEPOT (SLOW RELEASE) ANTIPSYCHOTICS: These are long-acting antipsychotic drugs, given as deep intramuscular injections to patients who improve with drugs but cant take it orrally

(¼ - ½ the dose) to check patient’s tolerability. Depot injections are released slowly in 1 – 8 weeks - Risperdal consta:25-50 mg./2weeks. -Zuclopenthixol decanoate ( Clopixol ) : 200 – 600 mg. /month.

Toxic Effect: Neuroleptic Malignant Syndrome (NMS) , Recent memory: loss ( early) dementia but may occur in normal elderly and because of medications side effect

Delirium Control mental and physical disturbance

contraindicated in Lewy Body Disease

SLE, MS) is associated with predominance of manic episodes and frequent psychotic symptoms. Antipsychotics (e.g. olanzapine 10mg) can be given to control such complications.

CNS Stimulants tr Symptomatic use of an antipsychotic medication e.g. olanzapine

side effect Depression ,,,, . LITHIUm may potentiate extrapyramidal side effect

clozapine side effect hypersalvation , myocarditis , ileus

DEPRESSION assessment

LOW ENERGY,PSYCHOMOTOR re=DOWN CAST GAZE HELPLESSNESS(B) =AKINESIA (B) =MUTENESS (B)=STUPOR STATE =numbness, insensibility").

ISOLATION-ANHEDONIA e lack of intrest worst core of sever

(PESSIMISSIM): pastSELF BLAME-unjustifiable GUILT FEELINGS Future: gloomy preoccupations; hopelessness, helplessness

PESSIMISSIM-HOPELESSNESS -DEATH WISHES (E)-SUICIDE IDEAS, PLANS, ACTS

diurnal VARIATION OF mooD (E) worse in the morning)

SLOW THINKING (T)=POOR ATTENTION,CONCENTRATION & MEMORY (C),In elderly PSEUDODEMENTIA=demintia with deppresion

LOW LIBIDO (Bio)=SEXUAL DYSFUNCTIONS (Bio),-and /or impotence. Change in bowel habit (usually constipation). amenorrhea()MARITAL PROBLEMS

INCREASED SLEEP (Bio)\ DECREASED SLEEP (Bio)= EMW (Bio)=earlymorning waking=g (terminal) insomnia waking 2 - 3 hours before the usual time, this is usually associated with severe

Obsessional symptom

Constipation -

:hypersomnia2 -Increased appetite or significant weight gain3-leaden paralysis or sensitivities of the legs that extend far beyond the mood disturbance episodes

interpersonal rejection sensitivity that extends far beyond the mood disturbance episodes

≥ 2 years history of chronic low mood.  No remission periods more than two months.  During low mood there should be ≥ 2 out of the

dysthymic disorder complicated by major depressive episodes (double depression)

insidious onset before age 25; the course is chronic. Some patients may consider early onset dysthymic disorder as part of life.

10 - 15 % recently delivered women develop disabling depression within 6 weeks of childbirth - if not treated may continue for six months or more

discrete periods of abnormal mood; low, ≥ 2 weeks of low mood/loss of interest

MDD is marked by chronic depression with symptoms lasting for as much as the whole life of the person. Additionally, MMD frequently occurs with other psychiatric problems, such as Bipolar Disorder or Anxiety Disorder. Those with MDD is with heart diseas

A. Presence of major depressive episode (s). B. Not better accounted for by schizoaffective disorder and is not superimposed on schizophrenia,

C. There has never been a manic episode, a mixed episode, or a hypomanic episode.

: Delusion that a patient has done something sinful, with excessive pathological feeling of remorse and guilt seen in severe depression.

Pseudo-dementia (Depression in the elderly): which is rapid onset after depression

Poverty of Speech -assment Poverty of thought

Delusion of poverty and impoverishment. 4. Persecutory delusion (patient accepts the supposed persecution as something he deserves, in contrast to schizophrenic patient).

Epidemiology of mdd: (more in women like any mood disorder).  Lifetime risk is in the range of 10 - 15 %.  Lifetime prevalence is in the range of 15 - 25 %.  The mean age of onset is about 40 years (25 - 50 years)

not uncommon. Child may not express his low mood verbally. so look for

usually self-limiting, but may become chronic or recurrent. Masked depression may present as a behavior disorder.

Depressive disorders were responsible for 40% of the burden of illness due to mental and substance abuse disorders.

Poor outcomes of the medical illness Increased mortality in cardiovascular disease, stroke, diabetes, and ?cancer Chronic medical conditions and depression are interrelated and that treatment of one condition can affect the outcomes for the other.

Four to five times greater levels of morbidity, premature mortality, health services use and health care expenditures compared to non- depressed patients with no GMC

Behavioural: Physical inactivity. Smoking. High carbohydrate & high fat diet.

mdd “count” all physical symptoms as part of depression even if possibly explained by the medical illness (to give patients, the benefit of doubt, by treating serious disabling illness like depression)

11 secs

Serum serology of hbv

HbsAg: ➔ Appears in serum 2 to 10 weeks. ➔ Persistence of HBsAg for >6 months implies progression to chronic=presistent carrier HBV infection. ➔ In self-limited acute hepatitis, HBsAg usually becomes undetectable after 4-6 months. ➔( The disappearance of

HBsAg → infection (carrier): surface antigen' -whern its disappear = non invective

HBeAg → viral replication

Viral load: HBV DNA → viral replication QUANTITATIV: - measured by PCR; if it persists > 6 weeks, patient is likely to develop chronic disease

Anti-HBs → immunity: n or after clearance of HBsAg, usually detectable 1 to 3 months after infection.

Anti-HBe → seroconversion= low infecctivity

. Anti-HBc (Hepatitis B core antibody) 1st ab → exposure to actual virus (IgM = acute): - Assay of IgM & IgG combined. - Useful because it may be the only serologic marker of HBV infection during the “window peek” in which HBsAg is disappearing,

The accurate diagnosis of acute hepatitis B require testing with immunoglobulin (Ig) M antibody to hepatitis B core antigen (HBcAg) (IgM anti-HBc)$

Coexistence of HBsAg and anti-HBs in serum has been reported in approximately 25% of HBsAg-positive persons and occurs more commonly in persons with chronic hepatitis B than in those with acute hepatitis B.

IgM class is usually detectable for 4 to 6 months after an acute episode of hepatitis or during exacerbation of chronic hepatitis B and rarely for up to two years.

antibody to HBeAg (anti-HBe)-=low infectivity

HbeAg ➔ Persistence of HBeAg three or more months after the onset of illness indicates a high likelihood of transition to chronic HBV infection.

80% of HBsAg-positive mothers who are HBeAg -positive transmit the disease to their offspring$$

after serology LFT, U/S liver, PCR,

how to deal with hbv patient? Measure for Family Contacts, screen and vaccinate the negative ones Referral to hepatologist, No blood donation

people who are HBsAg +ve can have sexual intercourse with their partners. normally if partner is vaccined

-the partner should receive a hepatitis B vaccination series (3 doses at 0, 1 month, & 6 months), then 1-2 months after finishing the series he/she should be tested for immunity against Hep B, if immune they can have intercourse without condom.

if hb core ab + but others nigative : Interpret the results: • H/O chronic exposure to HB virus

2- May be distantly immune and test is not sensitive enough to detect very low level of anti-HBs in serum.

4- May be a false positive anti-HBc.

Diagnosis: Hepatitis B surface antigen (HBsAg) o There is a good chance that the body will get rid of hepatitis B virus on its own within 6 months.

the infection. They will also have total antiHBc antibodies which means that this person was exposed to the virus; so he is immune by previous infection. (If HBc is not there and the patient is
immune, it means he is immune by vaccination). , HBe

• Newborn of HBsAg-positive mothers (MCQ): This will protect 95% of the kids$

Hepatitis B Immunoglobulins passive (within 12 hours of birth)

Vaccine

Older children: antiviral medications however most of these drugs are not effective and the hepatitis B stays with them until adulthood. So, Wait & observe (spontaneous recovery, new better antiviral medications)

core

anti hbc and hbs =history

acte HBsAg Anti-HBc igm , maybe HBV DNA

low level anti hbc positice =chronic

anti hbc only resolve most common2- fp 3- low level chronic

Inactive chronic infection

lazy

specific

, , E.g. of passive vaccine: if a pregnant mother is + ve for Hepatitis B, we give the newborn baby immunoglobulins (because the active vaccine takes time + already the mother's ,vaccine Interference with Immunoglobulins bc active , Hepatiti

Acute hepatitis, supporative

,, 89. An 11 month old infant recently arrived from an asian country, his status is unknown. Mother is positive hepatitis b surface antigen. What is the most appropriate vaccine infant should receive? B. HBIG (1 dose) and hepatitis b vaccine (3 dose withi

Note: Hepatits B virus is NOT a contraindication of brestfeeding because the babies are given immunoglobulin and vaccinations directly after birth if the mother is HBsAg positive.$ ,.

110- A pregnant lady Hip B: B. give immunolobunolin and Hep b vaccine in first 12 hours ,, - HepB +ve mom gave birth the child should receive: (1 answer) A. HBIG and vaccine at birth

acute and window ↑ (ALT > AST)

“Window period”maybe Anti-HBe

igm first then igg

HBV DNA window maybe

history Anti-HBe , igg

Active chronic infection hbsag , hbeag , igg , dna >2000 iu ml , alt >ast maybe

dna >2000 iu ml , alt >ast maybe

Inactive chronic infection hbsag , anti hbe , igg , hbv dna less or = 2000

Anti‑HBe Indicates long-term clearance of HBV

Screening: HBsAg (detectable 1–5 months after infection)

isolation

maybe

cirrhosis, cellular dysplasia → HCC

start

infectious

common

acute

normal child at birth , 2 , 4 , 6 passive

core

wand

antibody

Management of Hypertension

less120-80 reasses after1 year

Treatment of hypertension depend on the type of hypertension, comorbidity, the cause and the age of pt

120-129-less80 : lifestyle if they didn’t treat, within 0.5 - 2 years they will develop hypertension.

if there is no Atherosclerotic Cardiovascular Disease or 10yr cvd risk }Lifestyle Intervention In high risk patients ..if yes two in the begining tr like more140

Regular physical exercise : 30 min of moderate-intensity aerobic exercise 5-7 days/week

over 55yr or african amercan = ccb or thiazide like drugs= indapamide sr

under 55 yr: acei or arb

lifestyle and medication - reasses after 1month..these bellow are best initial

acei+ccb+thiazide in one pill

arb or acei)+ccb+thaiazide all in one --+ further duiritics or alpha or beta blockers

Hypertensive Emergency:Admitted to ICU and treat with IV administration.

Malignant (accelerated) hypertension : Need for ICU and treat with IV

55% of participants on medication for hypertension had their blood pressure uncontrolled.

Congestive heart failure : Thiazide, ACE-1, Aldosterone antagonist , BB

Diabetes Mellitus proteinuria : (ACEi,or ARB same effect ),NO

Chronic kidney disease : ACEi, ARBs, Thiazide

Stroke incidence will reduce 35 to 40% ● Myocardial infarction will reduce 20 to 25% ● Heart failure will reduce 50% ● Renal failure will reduce 35 to 50%

dult aged ≥18 years with hypertension t lifestyle interventions (continue throughout management).

Age ≥60 years Blood pressure goal SBP <150 mm Hg (or)DBP <90 mm Hg

Nonblack Initiate thiazide-type diuretic or ACEI or ARB or CCB, alone or in combination.a

all ages CKD present with or without diabetes Blood pressure goal SBP <140 mm Hg DBP <90 mm Hg

Select a drug treatment titration strategy A. Maximize first medication before adding second or B. Add second medication before reaching maximum dose of first medication or

if At goal blood pressure? Continue current treatment and

if not Reinforce medication and lifestyle adherence. For strategies A and B, add and titrate thiazide-type diuretic or ACEI or ARB or CCB (use medication class not previously selected and avoid combined use of ACEI and ARB).

if not goal Reinforce medication and lifestyle adherence. Add and titrate thiazide-type diuretic or ACEI or ARB or CCB

not At goal blood pressure?

Up to 65% of Americans with hypertension do not achieve adequate blood pressure control.

All Anti hypertensives are taken at night to prevent non dipping except diuretics which are taken in the morning

gestational htn hydralazine , dihydropyridine

dm In Microalbuminuria and Nephropathy (Renal damage) lower BP to ≤ 130/80

e Isolated Systolic • Thiazides , ccb

ifestyle changes “weight loss is the most effective” and any modifiable risk factors, such as obesity or smoking, should be controlled)

Adopt DASH eating plan Consume a diet rich in fruits, vegetables, and low fat dairy products with a reduced content of saturated and total fat. , reduce 8-14 mmHg in sbp

Physical activity Engage in regular aerobic physical activity such as brisk walking (at least 30 min per day. most days of the week). 4-9 mmhg red in sbp

The amount of blood pressure reduction is the major determinant of reduction in cardiovascular risk

diabetes management

to improve symptoms of hyperglycemia and to minimize the risks of long-term microvascular and macrovascular complications

education - Self-assessment USE DSMES GLUCOMETER , CGM , REVIEW INSULIN PUMP SETTING of glycaemic control: Insulin-treated patients should be taught to monitor blood glucose using capillary blood glucose meters, and to use the results to guide insulin do

Therapeutic goal $ : The target HbA1c depends on the patient. Early on in diabetes (i.e.patients managed by diet or one or two oral agents), a target of 48 mmol/mol (6.5%) or less may be appropriate,(7.5%) may be more appropriate in older patients with pr

In new cases of diabetes, adequate glycemic control can be obtained by diet and lifestyle advice alone in approximately 50%

reducing alcohol consumption and stopping smoking, are important but difficult for many to sustain first line

(first-line) drug therapy is with oral Metformin

Sulfonylureas

Thiazolidinediones provide no clear benefit over the other hypoglycemic medications

Nateglinide and repaglinid are stimulators of insulin release in a similar manner to sulfonylureas, but do not contain sulfa. They do not add any therapeutic benefit to sulfonylureas

Alpha glucosidase inhibitors (acarbose, miglitol)

Incretins

Insulin is added if the patient is not controlled with oral hypoglycemic agents -( First drug to give if patient came with HBA1c >10% is premixed insulin. $$

Prevent Complications

Patients with prediabetes (A1C 5.7% [39 mmol/moll, IGT, or IFG) should be tested yearly. 3. Women who were diagnosed with GDM should have lifelong testing at least every 3 years.

Prevention Or Delay Of Type 2 Diabetes Recommendation: At least annual monitoring for the development of type 2 diabetes in those with prediabetes is suggested. - Lifestyle Interventions

Metformin therapy for prevention of type 2 diabetes should be considered in those with prediabetes, especially for those with BMI ≥35 kg/m2, those aged <60 years, and women with prior GDM.

or more of moderate-tovigorous intensity aerobic activity per week, spread over at least 3 days/week, with no more than 2 consecutive days without activity. Shorter durations (minimum 75 min/week) of vigorous- intensity or interval training may be enough

A1C test at least two times a year in patients who are meeting treatment goals (and who have stable glycemic control). , quarterly in patients whose therapy has changed or who are not meeting glycemic goal

less than 6.5 Appropriate patients might include those with short duration of diabetes, type 2 diabetes treated with lifestyle or metformin only, long life expectancy, or no significant cardiovascular disease.

cont complications, extensive comorbid conditions, or long-standing diabetes in whom the goal is difficult to achieve despite diabetes self-management education, appropriate glucose monitoring, and effective doses of multiple glucose-lowering agents inclu

cont Peak postprandial capillary plasma glucoset <180 mg/d12` (10.0 mmol/L)

Blood pressure should be measured at every routine clinical visit. Patients found to have elevated blood pressure (≥140/90 mmHg) should have blood pressure confirmed using multiple readings, including measurements on a separate day, to diagnose hypertensi

In asymptomatic patients, routine screening for coronary artery disease is not recommended as it does not improve outcomes if ASCVD risk factors are treated. Consider investigations for coronary artery disease in the presence of any of the following: atyp

Consider aspirin therapy (75–162 mg/day) C

n patients with diabetes <50 years of age with multiple other risk factors (e.g., 10-year risk 5–10%), clinical judgment is required

Statin without adding anything else , At least once a year, assess urinary albumin (e.g., spot urinary albumin-to-creatinine ratio) and eGFR in patients with type 1 diabetes with duration of ≥5 years, in all patients with type 2 diabetes, and in all pat

cont The screening is done by using a camera “non mydriatic fundus camera”. The camera will take a picture and the picture will be sent to computer and the doctor will look

cont If the retina is ok then the screening is done every year. If mild non PDR → done after 6 months. If it’s severe non PDR, PDR or macular edema → refer to laser.

If there is no evidence of retinopathy for one or more annual eye exam and glycemia is well controlled, then exams every 1–2 years may be considered. If any level of diabetic retinopathy is present, subsequent dilated retinal examinations should be repeat

Women with preexisting type 1 or type 2 diabetes who are planning pregnancy or who are pregnant should be counseled on the risk of development and/or progression of diabetic retinopathy.

All patients should be assessed for diabetic peripheral neuropathy starting at diagnosis of type 2 diabetes and 5 years after the diagnosis of type 1 diabetes and at least annually thereafter.

Refer patients who smoke or who have histories of prior lower-extremity complications, loss of protective sensation, structural abnormalities, or peripheral arterial disease to foot care specialists for ongoing preventive care and lifelong surveillance.

DM pt on Metformin with HbA1c above target, Establieshed ASCVD or CKD. • Without established ASCVD or CKD: • To minimize hypoglycemia • To promote weight loss or minimize weight gain • Cost is a major issue

without established ascvd or ckd1- to reduce weight : GLP 1 OR SGLT2 , if not target add the other drug i

to minimize hypoglycemia ddp-4 or glp1 ra or sglt2i or tzd if note target add other from above

ascvd predominant glp1 or sglt all with proven reduce cvd if

hf or ckd: PREFERABLY SGLT2I if not tolerated or egfr less than adequate (ADD)glp1 ra , all proven ckd or cvd benifit

If HbA1c still above target despite dual/triple therapy, What to do? Consider GLP-1 RA in most prior to insulin. •

dont mix dpp4 with glp1 , HbA1c still above target despite adequately titrated basal insulin OR once basal insulin > .7 – 1.0 IU/kg OR FPG at target, What to do?

Xeroderma Pigmentosum

Defective Nucleotide Excision Repair

Extreme Light Sensitivity

Dark Freckles on Skin

Pale, Dry Skin

Susceptible to UV Rays A and B

Corneal Ulcers

Increased Risk of Skin Cancer

Some Patients Present Progressive Neurodegeneration

2 mins

Hyperchylomicronemia (Type I Familial Dyslipidemia)

Autosomal Recessive

Lipoprotein Lipase Deficiency (LPL)

Altered Apolipoprotein C-II (Apo C-II)

Increased Chylomicrons

Increased Cholesterol

Increased Triglycerides

Pancreatitis

Hepatosplenomegaly

No Increased Risk for Atherosclerosis

Eruptive/Pruritic Xanthomas

Milky White Appearance of Blood When Drawn

3 mins

Familial Hypercholesterolemia (Type IIa Familial Dyslipidemia)

Autosomal Dominant

Defective or Absent LDL Receptors

Defective Apolipoprotein B-100 (ApoB-100)

Increased LDL

Decreased HDL

Type IIb also has Increased VLDL

Accelerated Atherosclerosis

Achilles Tendon Xanthomas

Xanthelasma

Corneal Arcus

4 mins

Dysbetalipoproteinemia (Type III Familial Dyslipidemia)

Autosomal Recessive

Defective Apolipoprotein E (Apo E)

Increased Chylomicrons

Increased VLDL

Premature atherosclerosis

Tuberoeruptive xanthomas

Palmar xanthomas

3 mins

Hypertriglyceridemia (Type IV Familial Dyslipidemia)

Autosomal Dominant

Hepatic Overproduction of VLDL

Related to Insulin Resistance

Increased VLDL

Increased Triglycerides (> 1000 mg/dL)

Acute Pancreatitis

Eruptive Xanthomas

Increased Risk for Coronary Artery Disease (CAD)

Increased Risk of Peripheral Vascular Disease

3 mins

Live Vaccines

Varicella Zoster Virus (VZV)

Sabin Polio (Oral)

Smallpox

Yellow Fever

Influenza Intranasal

MMR

MMR: Only Live Attenuated Vaccine That Can Be Given To AIDS Patients

Induce Humoral And Cell Mediated Immunity

May Revert To Virulent Form

Do Not Require Boosters

4 mins

Killed Vaccines

Induce Humoral Immunity

Require Booster Shots

Influenza (Injected)

Salk Polio (Injected)

Hepatitis A

Rabies

3 mins

Subunit Vaccines

Consist of Specific Parts of a Pathogen

Hepatitis B Antigen

Human Papillomavirus (HPV)

Pneumococcal Vaccine

May Require Boosters

Safe in Immunocompromised Patients

1 min

Toxoid Vaccines

Consist of Toxins Released From a Pathogen

May Require Boosters

Safe In Immunocompromised Patients

Corynebacterium Diphtheriae Vaccine

Tetanus Vaccine

Bordetella Pertussis Vaccine

2 mins

Streptococcus Bovis

Group D Strep

Catalase-Negative

Gram Positive Cocci

Won't Grow in 6.5% Salt

Grows In Bile

Endocarditis

Bacteremia Associated With Liver Disease

Bacteremia Associated With Colon Cancer

3 mins

Leptospirosis and Weil's disease

Prevalent Among Surfers In Tropics

Leptospira interrogans

Spirochete

Hooked Shaped Ends

Water Contaminated With Animal Urine

Myalgias, Especially Of Calves

Flu-like Symptoms

Photophobia

Conjunctival Suffusion

Liver And Kidney Dysfunction

Jaundice

Hemorrhage

Anemia

3 mins

Trichinella spiralis

Nematode

Undercooked Meat (Especially Pork)

Larvae Enter Bloodstream And Encyst In Striated Muscle

Nause And Vomiting

Myalgia

Fever

Eosinophilia

Periorbital Edema

Albendazole And Prenidonse

2 mins

AV Heart Blocks

First Degree: PR> 200 Milliseconds

No Treatment Needed

Mobitz I (Wenkebach): Progressive Lengthening of PR Intervals Leading to Dropped Beat

Exercise Improves, Vagal Maneuvers Worsen

Mobitz II: Dropped Beats With No Preceding PR Prolongation

Atropine

Electrical pacing

Third Degree (complete): P Waves and QRS Beat Independently

Treated With Pacing

Lyme Disease Can Cause 3rd Degree Block

2 mins

Brugada Syndrome

Defective Myocardial Sodium Channels

Predominance in Asian Males

Autosomal Dominant

Pseudo-Right Bundle Branch Block Pattern

Persistent ST Elevations in Leads V1-V2

Risk of VTACH and Sudden Cardiac Death

Syncope

ICD

Antiarrhythmics

3 mins

Foregut Blood Supply and Innervation

Pharynx

Lower Esophagus

Proximal Duodenum

Liver

Gallbladder

Pancreas

Spleen

Vagus Nerve

Celiac Artery

3 mins

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