IM 2 Flashcards
CF-5 65 yo f brought to ER by family for increasing confusion and lethargy ofr the past week. She was recently diagnosed with small cell cancer of the lung. She is not taking any medications. Her BP 136/82 P84 R14 and labored, afebrile. On examination, difficult to arouse and reacts only to painful stimuli. No motor deficits, DTR are dec symetrically. Remander of exam is normal, normal JVP no edema. Labs sNa 108 sK 3.8 BC 24 BUN 5 Cr 0.5 SOsm 220 and UOsm 400 CT of brain WNL. Dx? next step? complication of therapy?
Dx: Coma/Lethargy 2’ to severe hyponatremia -> SIADH
NS: Hypertonic Saline
Complication: Osmotic Cerebral Demyelination (central pontine myelinosis)
S Osm?
280-300
Most common electrolyte disturbance among hospitals?
Hyponatremia <135
Clinical manefestation of hyponatremia?
Related to osmotic water shift leading to cerebral edema:
lethargy confusion siezures and coma
HyperOsm Hyponatremia
More dangerous and related to solute that is confined to extracellular space: glucose/mannitol.
Drawing solutes out and leadint to “relative” HypOnatremia.
Glucose HyperOsm State:
For every 100mg/dL increase, 1.6 mmol/L decrease in serum sodium.
Pseudohyponatremia?
sNa and tonicity are normal.
High serum protien levels or high lipid levels interfered with the measurement of serum sodium level.
Check the measured and calculated sOsm
Kidney free water excretion capacity?
kidney capacity to excrete free water is 20L/d
difficult to overwelm the system in primary polydipsia
Hypotonic Hyponatremia signs/symptoms of water loss?
vomiting, diarrhea, sweating/ dry MM, dimished U output, flat neck veins.
Hypervolemic signs/symptoms?
edema, elevated JVP, CHF, Cirrhosis, Nephrotic syndrome
Euvolemic hyponatremai?
Most commonly caused by SIADH -inapproprieate secreation seen in Pulm Dz, CNS Dz, Pain, Post OP, Paraneoplatic.
ADH?
Diagnose SIADH
Urine?
Labs?
ADH is a neuropeptide that concentrates urine. Water retention.
Exclusion, Hypoosmolar but Euvolemic:
Uosm >150 (non dilute)
UNa >20 and normal adrenal and thyroid function.
Other labs: low BUN low Uric Acid
Treat SIADH
unless severe: water restriction
Severe: symptomatic
Hypertonic saline
U Osm what does it tell you?
Kidney capable of excreating free water normally?
Max Dilute: 150-200: Urine max concentrated
Free water excretion is impaired you have a UOSm of >200? What does that mean?
1) Hypothyroidism
2) Adrenal Insufficiency
(Thyroid H and Cortisol are permissive for free water excretion)
NOTE: Addison’s Dz patient lack aldosterone.
Symptoms of osmotic cerebral demylination
Quadraplegic, pseudobulbar palsies and “locked-in” syndrom, coma or death
correct sodium by 0.5-1mEq/hr
mineralcorticoid def will do what to K?
K will be low.
24 year old man develops siezures following and emergent slenectomy after a car accident. sNA 116 and is corrected to 120mEq/L over the next three hours with hypertonic saline. Which factors led to his hyponatremia?
STRESS:
Elevation of serum vasopressin
56 yo M presents to the doctor for the first time complaining of fatigue and weight loss. He has never had any health problems, but he smoked a pack of cigs a day for 35 years. He is a day laborer and currently homeless and living in a shelter. PE: low normal blood pressure, skin hyperpigmentation, and digital clubbing. Appears euvolemic. Blood tests are drawn and follow up in 1 week. Lab calls that night and informes you that the patients sNa is 126 sK 6.7 Cr WNL BCb Low. Cause of hyponatremia?
Adrenal Insufficiency
83 yo F comes to your office complaining of headache and mild confusion. PMH is remarkable only for HTN, controlled with hydroclorothiazides. Her examination and lab test show no signs of infection, but her sNa 119 and plasma Osm 245 mOsm/kg she appears hypovolemic. Best initial therapy?
Infusion of normal saline.
Hypovolemic hyponatremia secondary to diuretic use.
58 yo man has undergone a lenghty colon cancer surgery. On the first day post op, he is noted to have significant hyponatremia with a Na 128. You suspect hyponatremia is due to intravenous infusion of hypotonic solution. Which of the following lab findings support your dx? uNa will be? uOsm? sOsm? sK?
1) kidneys excrete water retain Na: uNa low uOsm low 2) Excess water: sOsm low, low electrolytes -low K
CF-6 42 yo M in ER after sudden onset severe retrosternal chest pain that began an hour ago while he was at home mowing his lawn. He describes the pain as sharp, constant, unrelated to movement. It was not relieved by three doses of sublingual nitroglycerin administered by the paramedics while en route to the hospital. He has never ad symptoms like this before. His only medical history is hypertension, for which he takes enalapril. There is no cardiac dz in his family. He does not smoke, drink alcohol, or use illicit drug. He is a bball coach and very active. PE: tall long arms and legs, appears comfortable and diaphoretic; lying on the stretcher with eyes closed. afebrile P118 BP156/100RA 188/94LA chest: BCTA with pectus excavatum. HR tachy/regular with soft early diastolic murmur at right sternal border. Abd is benign and neuro is nonfocal. Xray show widened mediastinum. Dx? NS?
Aortic Dissection,
NS: control his BP
(IV-BB and perform noninvasive imaging, TEE, CT angio or MRI.)
Abdomial Aortic Aneurysm definition:
Dilation of >1.5 normal diameter of aorta. (nl: 1.5cm)
Most are abdominal below the renal arteries.
Aortic Dissection definition:
Tear or ulceration of aortic intima that allows pulsatile aortic flow to dissect longitudinally along elastic planes of media, creating false lumen or channel for blood flow. Sometimes reffered to as a dissecting aneurysm, although term is misleading because the dissection typically produces aneurysma dilation rather than the reverse.
3 layers of aorta?
intima, media and adventitia
Factors predisposing to A-D?
Cystic degeneration of elastic media seen in connective tissue dz: Marfans, Ehlers-Danlos.
Other factors: HTN, aortic valve abnormalities, pregnancy and artherosclerotic dz.
What is happening during an aortic dissection?
Sudden intimal tear/rupture followed by dissecting hematoma within aortic media, separating the intima from the adventitia and propagating distally.
Complications of A-D?
Intimal flap causing clots and end organ damage.
Rupture: Tamponade, Pleural space, exsanguination. Aortic regurge/HF
Clinical pain?
Why is this important?
ripping, tearing of the chest radiating to the back.
Anticoagulation or thrombolytics with dissection may be devistating.
Look for new onset aortic murmer of insufficiency.
Classification A-D? Why is this important?
Type A - ascending and can involve other parts
Type B - non asscending.
Type A = Surgical Therapy wo 90% mortality
Risk of rupure?
related to size of aneurism:
6cm ~15% (elective surgery)
59 yo M severe chest pain radiates to his back. Brachial pulses appear unequal. Hemodynamically stable, C-Xray wide mediastinum. Which of the following is the next best step?
Control BP, get CT contrast
45 yo F new onset aortic regurge, found to have aortic dissection of ascending aorta and aortic arch by echocardiography. Relatively assymptomatic. Best management?
Surgical Correction
75 yo M US for suspected gallbladder dz found incidentally to have 4.5cm abdominal aneurysm of the aorta. Best manangment?
Serial US examinations every 6mths,
AAA 5.5cm or greater surgery, if less then follow.
Low risk for rupure 1-2%
45 yo M concerned because his father died of ruptured abdominal aortic aneurysm. Evaluation, he is found to have bicuspid aortic valve. What does that say about his risk?
Not at increased risk.
Risk factors are smoking HTN, PVD.
CF-7 32yo M infected with HIV, last CD4 was unknown, presents to ER with temp 102.5’F Diagnosed with HIV 3yrs ago when presented with oral thrush. Started HAART and stayed on regimen for 10mths, stopped due to job loss. Last 2-3 weeks has had fever and nonproductive cough, SOB with mild excertion, FE: BP 134/82 P110 R28. O2 Sat 89% rest, 80% when he walks, breathing is labored. Lungs clear to auscultation, white patches cover buccal mucosa. Otherwise unremarkable. Labs: 2800 cells/mm. sLDH 540 U/L. Radiograph is shown diffuse bilateral infiltrates. Diagnosis? NS?
Dx: AIDS and Pneumocystis pneumonia. Lack of sputum and elevated LDH is suggestive of PCP. Must suspect other resp infextions.
NS: Stabilize pt, and Arterial Blood Gas-impact his treatment.
Arterial Ox less than 70mmHg or Alveolar-arterial gradient >35mmHg suggest worse prognosis and corticosteroids may be helpful.
Tx with TMP-SMX.
Define AIDS?
CD4 less than 200 cells/mm3
or
Diagnosis of AIDS defining illness in HIV postive pt.
Define Pneumocystic Jirovecii?
Fungus that causes pneumonia in immunocompromised pt, especially those with HIV and CD4 less than 200c/mm
Normal CD4 levels?
600-1500
Acute HIV syndrome?
Acute HIV Synd: 30% of patients first infected with HIV will develop suden onset mono-like symptoms:
macular rash, fever, headaches, lymphadenopathy, pharangitis.
Rest will have a clinically latent period of 8-10 yrs.
CD4 <500
susceptible to infections, pneumonias, TB, vaginal candidiasis, herpes zoster.
CD4 <200
Immunocompromised (acquired immunodifficiency sydrome) Pneumocystis Jirovecii, Cryptococcosis, Cryptosporidiosis Toxoplasmosis, Histoplasmosis,
CD4 <50
Disseminated Histo and Mycobacterium avium,
CMV; retinitis, colitis and esophagitis, necrotizing adrenalitis or
CNS lymphoma.
Most common opportunistic infecction?
Pneumocystis pneumonia PCP hard to diagnose - wide range of presentations:
dry cough, hypoxemia
normal film -> diffuse infiltrates, cycts or blebs.
Spontaneous pneumothorax.
Diagnose PCP?
Giemsa or Silver Stain, require induction of sputum with aerosolized hypertonic saline.
Elevated LDH: nonspecific marker used (histo and lymphoma also) LDH 250 -> or on TMP SMX ->unlikely
Treat PCP?
TMP-SMX, if allergic to sulfa
clindamycin with primaquine
or
Pentamidine
AIDS with chest Xray: Patchy Infiltrates and pleural based infiltrates.
TB and cryptococcal lung dz NOTE a negative PPD does not rule out TB in Immunocomp host
AIDS with chest Xray: Diffuse infiltrates
PCP, mycobacterium kansasii, disseminated histo, MAC
AIDS with chest Xray: Cavitary lesions
TB, PCP and coccidiomycosis
Most common causes of pneumonia in AIDS?
Are still community acquired pneumonia
Most common CNS lesion in AIDS patient?
Cerebral Toxo
multiple lesions:, headache, siezures, focal neurological deficitis.
Major alternative is CNS lymphoma (EBV) -> SINGLE MASS LESION.
Mood disturbanc, headaches, visual disterbance? CSF WNL
Cryptococcal meningitis, chronic indolent infection.
Do a serum cryptococcal antigen or LP with india ink stain, cryto ag, or fungal cultures.
Tx IV-AmphoB and Fluconazole
CMV tx?
IV-Gancyclovir, foscarnet or Cidofovir
MAC tx?
Clarithromycin/Ethambutol and rifampin for weeks
Prophylaxis CD4 <200? 100? 50?
200: TMP-SMX 3x week.
100: TMP-SMX daily.
50: Clarythromycin 500mg daily or Azithromycin 1200mg weekly.
Prophylaxis discontinued when HARRT is initiated and CD4 levels recover.
Immune reconstitution syndrom?
worsening of symptoms after HARRT is initiated due to improved immune response.
32 yo W with 5yr hx of HIV infection noted to have CD4 count of 100c/mm. She is admitted to the hospital with a 2 week history of fever, SOB and dry cough. Diagnostic test would confirm diagnosis?
Silver stain of the sputum looking for PCP
Most likely organism to cause pneumonia in an AIDS patient?
Streptococcus Pneumoniae
44 yo W infected with HIV is noted to have a CD4 count of 180c/mm. Which of the following is recommended as a useful prophylactic agent in this patient at this point?
TMP-SMX
36 yo F with HIV is admitted with new onset seizures. CT of head reveals multiple ring enhancing lesions of the brian. Best therapy for this likely condition?
Sulfadiazine with pyrimethamine
CF-8 58 yo M present to ER complaint of severe pain in the left foot that woke him from sleep. History of chronic stable angina, hypercholesterolemia, HTN takes asprin, atenolol and simvastatin. Experienced pain in both feet with walked for several years, pain is gradually progressed so that he can now only walke 100 feet before he has to stop bc of the pain. He occasionally has experianced mild pain in his feet at night, but the pain usually gets better when he sits up and hangs his feet off the bed. This time the pain is more severe and did not improve, and now feels like the foot is numb and cannot move his toes. PE: afebrile, P72, BP125/74. HEENT: rt carotid bruit. Chest: BCTA Heart: RRR nondisplaced apical impulse, S4 gallop, no murmurs. His abdomen is benign, no tender masses. He has bilateral femoral bruits, palpable femoral and popliteal pulses bilaterally. Pedal pulses are diminished, present on right foot absent on the left. Left distal leg and foot are pale and cold to touch, slow capillary refill. Dx? Next Step?
Acute limb ischemia
(6p’s pain pallor pulseless parasthesias poiklothermia; paralysis if severe or persistent) thrombotic arterial or embolism from distant source.
NS: Lower Ext angiogram
calf pain with walking, resolution with rest. Pain at night while laying in bed relieved by dangling the legs.
classic for claudication, if pain during resting-> critical for critical limb vascular insufficiency
ankle brachial index
ratio of systolic bp in ankle to brachial, determined using US
Ratios from 0.41-0.90, Critical is <0.4
Perihperal arterial disease etiology?
affects 16% of people >55yo,
most important risk factors are smoking and DM.
Also, HTN, dyslipidemia, elevated homocysteine
exertional pain in buttock or thigh
aortoiliac dz:
listen for bruits, and feel for peripheral pulses, look for hair loss,
elevation of the soles/feet induces pallor in soles
symptomatic PAD mortality rate
50% in 10 years, smoking reduces the risk of fatal or nonfatal myocardial infarction by as much as 50%
Medications for PAD
Pentoxifylline, xanthine derivative enhances erythrocyte elasticity.
Cilostazol, phospherdiesterase inhibitor with vasodilatory and antiplatet properties - impoves maximal walking distance
Algorithm for suspected PAD or
ankle brachial index: ABI <90%
Treat cardiovascular risk factors: STOP SMOKING LDL < 100, BP <130/85, ACE I, ASA
Critical leg ischemia definition
<0.40 ABI, severe disabling claudication,
rest pain,
nonhealing ulcers
management is evaluation for bypass grafting or angioplasty
PAD in pt <40 heavy smoker
OBVI: AFFECTS UPPER/LOWER EXT
Thromboangiitis obliterans, or Buerger Dz inflammatory condition of small and medium arteries.
PAD in women with prerenal insufficiency
Fibromuscular dysplasia, likes to affect the renal and carotids.
Woman <40 Raynauds, arm claudication, fever, weight loss
Takayasu Arteritis, affecting the branches of the aorta likes the subclavian arties
Tx of acute arterial occlusion
RAPID RESTORATION: heparin prevent propigation, place the limb below the horizontal plane, without pressure applied to it. Surgical evaluation for thrombectomy, balloon catheter, intraarterial thrombolytic therapy (fibrinolytic)
49yo smoker with HTN, DM, hypercholesteralemia comes complaining of pain in calves when walking 2-3 blocks. Therapy that might offer the greatest benefit in symptom reduction and in overall mortality?
STOP SMOKING
31 yo male smoker with resting pain in legs and a nonhealing foot ulcer?
Thromboangiitis obliterans, Buerger Dz inflammatory condition of small and medium arteries. OBVI: AFFECTS UPPER/LOWER EXT
21yo female with fever, fatigue, and unequal pulses and blood pressures in her arms.
Takayasu Arteritis, affecting the branches of the aorta likes the subclavian arties
62yo man with livedo reticularis (reticulated net like pattern on skin) and three blue toes, including one with gangrene following cardiac catheterization.
Cholesterol Embolism
67yo woman noted to have significant peripheral vascular dz. She is evaluated by the cardiovascular surgeon but not felt to be a surgical candidate. Which of the following conditions is likely to be present in this patient?
Diffuse atherosclerotic dz, Surgery is reserved for severe symptoms after exercise and pharmacologic agents are not useful and quality of life is impaired.
CF-9 56yo M comes into your office as a new patient. 7 years ago at a work-related health screening, he was diagnosed with HTN and Hchol. At this time, he saw a physician who prescribed a diuretic and encouraged him to lose some weight and to diet and exercise. Since that time, the patient has not sought medical attention. During the past 2 mths, he has been experiencing occasional headaches, which he attributes to increased stress at work. He denies chest pain, SOB, dyspnea on excertion, paroxsysmal nocturnal dysnea. He smokes one pack of cigarettes per day and has done so since he was 15yo. He typically drinks two glasses of wine with dinner. On examination, the patient is obese, and you calculate his BMI as 30kg/m. His BP is 168/98 in the right arm and 170/94 on the left arm. BP did not change with changes in position. His heart rate is 84. He has no thyromegaly or lymphadenopathy. Fundiscopic examination reveals narrowing of the arteries, arteriovenous nicking, flame-shaped hemorrhages with cotton wool exudates. Cardiac examination reveals that his point of maximal impulse is displaced 2 cm left of the midclavicular line. There is an S4 gallop. No murmurs are auscultated. Lung and abdomen examinations are normal. Next Step?
1) HAS END STAGE ORGAN DAMAGE, evaluate other organs Renal Function - CMP and Cardiac - baseline ECG. 2) Patient is >160/100 placing him in STAGE II. Start 2-drug antihypertensive regimen that includes thiazide. 3) Lifestyle changes - STOP SMOKING!!!
Define Essential Hypertension
No known cause, and comprises 95% of all cases of HTN. (Sec HTN-5-10%)
Lifestyle Modifications:
Regular aerobic activity,
weight loss,
decreased salt intake,
increased intake of fruits and vegtables,
decrease total fats - saturated,
Moderate alcohol consumption ( no more than 1 glass per day for women and 2 glasses for men)
PreHTN:
120-139/ 80-89 Lifestyle Modifications unless cormobid condition then therapy
Stage I HTN:
140-159/90-99 Single antihypertensive
Stage II HTN:
160/100 at least 2 antihypertensives
Secondary HTN:
Elevated arterial blood pressure with known underlying cause: Onset 55,
malignant HTN: >3 medications to control, HTN suddenly uncontrolled, rising Cr level with the use of an ACE-I
Prevalence is 5-10% of all cases of HTN.
Onset 55,
malignant HTN: >3 medications to control, HTN suddenly uncontrolled, rising Cr level with the use of an ACE-I
Secondary HTN:
1) Renal: -Parenchymal (glom-nephritis, PC-RD, DM-Neph) -RenoVascular
2) Endocrine: OCP, Primary Aldosteronism, Cushings, Pheo, HyperThyroid, GH,
3) Misc: Coartication, Increased intravascular volume-posttransfuion, HyperCa, Medications (sympathomimetics, glucocorticoids)
Target BP?
135/85 unless DM or Renal Dz then <130/80
Why do we always use a Thiazide?
SHOWN TO DECREASE MORTALITY, unless contraindicated use with a Bblocker
Thiazide Diuretic
CONTRA: DM GOUT HYPOK. Mechanism sodium diuresis, volume depletion SE: HyperGLUC- hypoKalemia
Furosemide
CONTRA: GOUT HYPOK. SE HypoK-Ca HyperGlycemia-Uricemia
Potassium sparing Spironolactone
CONTRA: RF SE HYPERK, gynecomastia, diarrhea
Antiadrenergic
Clonidine, BB, Carvedilol
Clonidine
CONTRA: noncompliance. SE postural hypotension, drowsiness, dry mouth, rebound HTN with abrubt withdrawl. Stimulates alpha-2 vasomotor center of the brain
Metoprolol, Atenolol
CONTRA: Asthma, 2nd/3rd degree heart block SE: Bronchospasm, hyperlipidemia, GI symptoms, depression, erectile dsfunction. Blocks sympathetic effect of heart and kidney (renin)
Carvedilol
same as BB, but also direct vasodilator (alpha-beta blocker)
Hydralazine
CONTRA: severe coronary artery dz. SE: headache, tachycardia, angina, lupus like syndrome. Arterial vasodilation, produces reflex tachycardia
Nitroprusside
Cyanide Toxicity, muscle twitching, weakness, fatigue, nausea,
ACE I
CONTRA: RF, Bilateral artery stenosis, pregnancy. SE Leukopenia, pancytopenia, cough, angioedema, urticarial rash-hives, hyperkalemia, ARF
Losartan, Valsartan, Candesartan
CONTRA: RF, Bilateral artery stenosis, pregnancy. SE Leukopenia, pancytopenia, urticarial rash-hives, hyperkalemia, ARF
Amlodipine, Nifedipine (dihydropyridines)
CONTRA: HF, HEART BLOCK SE: Tachycardia, flushing, GI Side effects, hyperkalemia, EDEMA
Diltiazem, Verapamil (non dihydropyridines)
CONTRA: HF, HEART BLOCK SE: heart block, constipation
Drug of choice in pts with HTN, DM or heart failure
ACE I , if thiazide is added know that glucose may increase
Most common cause of secondary HTN?
Renal Dz
(older patient - renal artherosclerosis, young patient - fibromuscular dysplasi) look for secondary hypoKalemia (high aldosterone)
NS: captopril-enhanced radionuclide renal scan
Bilateral flank masses, flank pain, HTN and hematuria?
Polycistic Kidney dz
HTN and hypokalemia
primary hyperaldostronism
Other causes of secondary HTN
anabolic steriods, sympathomimetic drugs, tricyclic antidepressants, nonsteriodal anti infalmmatory agents, illicit drugs, cocaine, caffiene, tobacco
heavy snoring
obstructive sleep apnea, hypoxic, hypercarbic during sleep leading to systemic vasocontriction, systolic HTN, pul HTN
wide pulse pressure, warm skin, tremor, thyroid gland enlargment
hyperthyroidism, low TSH and elevated free T4
thinning of extremities with truncal obesity, supraclavicular fat pad, purple striae, acne, psychiatric symptoms
Glucocorticoid excess states, cushings
HTN, leg caudication, cold LE extremities, diminished or absence of femoral pulses
Coartication of the Aorta
headache, diarrhea, wheezing
Carcinoid Sydrome
anxiety, nervousness, tremor, pallor, malaise, nausea, vomiting
Pheochromocytoma
30yo female noted ot have blood pressure in the 160/100. Has increased obesity around the abdomen with striae. Bruising easily and has hirsutism. Dx?
Cushing syndrome, adrenal steroid overproduction
45yo M diagnosed with idiopathic HTN based on two bp 150/100 and 156/102. What would provide prognostic information?
End organ effects
34yo F is noted to be diagnosed with stage I hypertension and after an evaluation is noted to have no complications. Which of the following antihypertensive agents are generally considered first line agents for this individual?
Thiazide diuretics
45yo man with DM T2 noted to have blood pressure of 145/90 and 150/96 two separate occasions. Which of the following is the best initial therapy for this patient?
ACE I , if thiazide is added know that glucose may increase
CF-10 39yo found wandering the street, disoriented state. Confused and agitated, hx from wife: intermittent headache and palpitations, and lightheadedness and flushed skin when playing bball. 3 weeks ago, dx with HTN clonidine was started. Clonidine made him feel sedated so he was switched to metoprolol. VS: P110 R26 O2 98% BP 215/132 equal in both arms. Agitated and diaphortic, does not recognize his wife. Pupils dilated but reactive, papilledema and scattered retinal hemorrhages, no thyromegaly. Heart, lung andd abdominal examinations are normal. Pulses bounding, reflexes brisk and symmetric, slight tremulous. CT of head is negative for hemrrhage. Lab studies include normal leukocyte count Hgb 16.5 sNA 139 Cl 105 HCO3 29 BUN 32 Cr 1.3 Urinalysis is normal, drug screen is negative. Lumber puncture is performed and CSF no cells and normal protien and glucose. Dx? Etiology? Next step?
Hypertensive encephalopathy secondary to pheochromocytoma. Admit to the ICU, lower BP and closely monitor arterial pressure. Young man with severely elevated blood pressure, confusion, increased intracranial pressure, and/or siezures and NEG drug for cocaine and amphetamines.
DX of exclusion: stroke, subarach hmg, meningitis, mass lesions.
Lower BP by 25% initially
then lower bp to 100-110mmHg in 2-6 hours.
Once controlled continue to control the BP to 85-90.
Expect initial renal injury from low bp, but this is transient and will resolve over weeks.
MEN IIA:
Pheochromocytoma, HyperParathyroid, Medullary Thyroid Ca
MEN IIB:
Pheochromocytoma, Medullary Thyroid and Mucosal Neuromas
Hypertensive Emergency:
End organ effects, REDUCE BP IN 6 HRS
Hypertensive Urgency:
No end organ effects, slowly reduce bp over 2 days
Hypertensive Crisis what do you suspect?
Drugs: cocaine, clonide withdrawl, sympathomimetic agents
Underlying dz: Renovascular disease (artery stenosis), renal parenchymal disease (glomerulonephrtis), pheochromocytoma
Why does the actual number in BP not regulate your management in hypertensive emergencies?
Pts with chronic HTN have a compensatory mechanism for autoregulation with a rt shit of the curve. So, the number may be high but not significant in this patient. Previously normotensive worry about 160/100. FOCUS ON SYMPTOMS NOT NUMBERS.
What do you have to worry about in a patient with chronic htn, when lowering BP?
“Normalizing” BP may cause ischemia (renal, cardiac, cerebral) if they have been HTN and have Left shifted the curve.
Normotensive Cerebral Blood Flow?
Mean Arterial Pressure where this is constantly regulated?
In a normal, NON-chronic pt:
70ml/100g/min
Mean arterial pressure: 60-120
MAP: (2xDP + SP) /3
Most commonly used in hypertensive emergencies?
Sodium Nitroprusside, results in thiocyanate/cyanide toxicity if given for more than 2-3 days.
Decrease the preload?
Ideal in acute pulmonary edema: IV loop diuretics and vasodilators
AAA or Cardiac Ischemia use?
Labetolol
Cerebral ischemia?
CAREFUL, lowering can worsen symptoms
flushing, dilated pupils, diaphoresis in hypertensive urgency/emergency
pheochromocytoma-chromaffin cells, catecholamine producing.
1) serum elevated catecholamines
2) 24hr urine metanephrines, VMA and conjugated/free catecholamines.
Then locate (90% are in the adrenals)with CT, I-metaiodobenzylguanidine, octeotride and remove
Treament of HTN secondary to Pheochromocytoma?
Phenoxybenzamine, 1 week prior to sugery. Liberal salt diet due to contracted blood volume. Bblocker only after a Alpha blocker is started, may result in pulmonary edema.
Why salt diet?
Orthostatic HYPERTENSION, patient is still volume depleted but sympathetically active. Hence you give salt repleat volume.
Pheochromocytoma, whats the familial link?
RET protooncogene - MEN II
or VHL (hemangiomas: cerebellum/BS, kidney, retina)
or familial pheochromocytoma and neurofibromas
30yo man with chronic HTN presents to clinic having run out of his medication, clonidine. He has no coplaints and has a BP 200/140 mmHg. Which is the best management?
Restart the clonidine and recheck in 24-48 hrs, Pt is hypertensive urgency due to clonidine rebound.
80yo woman without history of HTN undegoes surgery for a hip fracture. BP on postop day 1 is 178/110 mmHg. Patient is asymptomatic except for hip pain. Best next step?
Start a Bblocker and monitor BP, and monitor closely.
61yo man with coronary artery disease complains of progressive orthopnea and pedal edema. Hospitalized with BP of 190/105. Cardiac enzyme levels and ECG are WNL. IV furosemide administered. Best next step?
ACE I, reduce afterload used to treat acute heart failure.
Avoid Bblockers in patients with CHF.
58yo woman with aphasia and right arm weakness of 8 hrs duration is seen in the ER. BP is 162/98. Best next step?
Observe the BP, HTN should not be acutely decreased unless markedly elevated In an individual suspected of having a stroke, concern for cerebral hypoperfusion and worsening brain ischemia.
CF-11 28yo man compaining of 5d history of nausea, vomiting, diffuse abdominal pain, fever to 101’F and muscle aches. Loss of appetite, tolerates liquids, no diarrhea. No significant medical history or family history, not traveled outside the US. 12 different lifetime partners, denies illicit drug use, drinks alcohol occasionally, not since illness began. No medications routinely, takes acetaminophen, 30 tblts for 2 days for fever and body aches since illness began. PE: T 100.8 P 98 BP 120/74. Jaundiced, chest clear to auscultation, heart rhythm is regular without murmurs. Liver percusses 12cm and is smooth and slightly tender to palpation. No abdominal distention or peripheral edema. Lab values Normal CBC, Cr 1.1, ALT 3440, AST 2705, TB 24.5, DB 18.2, ALKP 149 Albumin 3.0, prothrombin 14 sec. Dx? Immediate diagnostic tests?
Acute hepatitis, viral, toxic injury, possibly exacerbated by acetaminophen use. Immediate diagnostic test: Acetaminophen level. Pt has acute onset hepatic injury ans systemic symptoms, elevated hepatic transaminase and bilirubin levels are consistent wiht viral hepatitis or toxic injury.
Transaminases >1000
Excessive hepatic necrosis: toxic, viral and ishemia (SHOCK LIVER)
Transaminases <500
Alcoholic Liver AST:ALT 2:1
Define Chronic Hepatitis
Syndrome defined clinically by evidence of liver dz for at least 6 consecutive months.
MOST COMMON ACUTE VIRAL HEPATITIS IN THE US?
Hepatitis A
Hepatitis Virus that is very contagious and transmitted fecal oral?
Hep A and Hep E-(developing countries), both are self limiting and resolve in weeks. Pregnant and Hep E: Severe hepatic necrosis, fatal liver injury
Hepatitis virus usually transmitted sexually, also IV drug abuse, during birth?
Hepatitis B, 90% of infected newborns will develop chronic hep B - high risk for hepatocellular carcinoma. Adults: 95% recover without sequelae. 5-10% develop chronic hep B
Hepatitis virus transmitted by blood transfusion or intravenous drug use, rarely sexual contact?
Hep C
Usually diagnosed later as a cause of chronic hepatitis
Patient with history of chronic hep B now with liver deterioratin?
Hep D, superinfection requires Hep B to replicate.
Fulminant Hepatic failure: Induced by? What is seen? Labs? Prognosis?
Induced by Hep B or D, or drugs.
Characterized by rapid progression of encephalopathy from confusion or somnolence to coma.
Worsening coagulopathy: increased prothromin, bilirubin, ascites, peripheral edema, hypoglycemia, hyperammonemia and lactic acidosis.
Prognosis 80% mortality for comatose pts.
Diagnose Hepatitis A?
Anti-hepatitis A IgM
Diagnose Hepatitis B?
Acute- HBsAg then window period then anti-HBsAb.
Anti-HBc IgM (acute) HBeAg high level of replication.
Chronic hep C: perisistence of HepBsAg or HBeAg
Carrier-normal transaminases Chronic-elevated transaminases.
Diagnose Hepatitis C?
Hepatitis C RNA assay, Anti-HepC Ab (may take weeks to become positive)
Prevention of hepatitis A?
Hep A vaccine, efficacy of 90%, two doses 6mths apart. Indications: traveling to endemic area, postexposure prophylaxis given with hep A Ig to household and intimate contacts within 2 weeks of exposure.
Prevention of hepatitis B?
Hep B vaccine, efficacy of 90%, 3 doses over 6mths. Indicated in healthcare workers, universal infant vaccine. Hep B Ig, given after exposure along with vaccine.
Interferon, lamivudine?
Interferon for B/C, lamivudine for B
Acetaminophen Hepatic toxicity occurs when?
acute ingestion of 10g or more, lower doses in patients with known hepatic injur or P450 inducer.
P450-metabolite that binds up glutathiione.
Acetaminophen toxicity management?
Acetaminophen is measured at 4 and 24 hrs after acute ingestion and plotted on normogram to predict tx. If levels that predispose to hepatic injury tx: charcoal and N-acetylcysteine (cystiene replenishes glutothione) started within first 10 hours and continued for 72hrs. Avoid hepatotoxic drugs.
25yo stuck with needle on patient known to have hepatitis B and C, HIV negative. Baseline labs show HBsAg negative, Anti-HBsAb positive, anti-HBc IgG negative. Hepatitis status?
Prior vaccination with hepatitis B vaccine
Exposure prophylaxis should the student receive?
Reassurance, there is no effective prophylaxis for hepatitis C exposure
18yo female takes 4g of acetaminophen, approximately 8 hours previously. Acetaminophen level is 30ug/mL. Best next step?
Observation
