Boards Part 2 Flashcards

1
Q

Pacemaker for

A

• Third degree AV block or equivalent
(e.g., first degree AV block with LBBB and RBBB)
• Heart rate 3 seconds
• Sick sinus syndrome with symptoms (e.g., syncope)

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2
Q

Most common cause of tachycardia

A

re-entry

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3
Q

types of supraventricular tachycardia

A
  • Sinus tachycardia
  • Paroxysmal supraventricular tachycardia (PSVT)
  • Sick sinus syndrome (SSS)
  • Wolff-Parkinson-White/Lown-Ganong-Levine (WWW/LGL)
  • Atrial flutter
  • Atrial fibrillation
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4
Q

sinus tachycardia cause and tx

A

irritable SA node or atrial focus

Treat primary disorder (rehydrate, o2)

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5
Q

PSVT tx

A
Vagal manuevers (80%)
IV Adenosine or overdrive pacing

BB, CCB, Dig are preventitive

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6
Q

Short PR interval (<.12 sec)
Congenital accessory AV pathway

Tx for it

A

Wolff-Parkinson Whjite

Radiofrequency ablation is TOC

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7
Q

Sawtooth pattern seen in mitral stenosis, pericarditis and ARF

A

Atrial flutter

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8
Q

Irregularly irregluar rhythm

tx

A

Atrial fib

Rate control with BB or CCB
CVA proph with warfarin if chronic

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9
Q

> 3 cons PVCs

A

Vent Tachycardia

can be paired, multifocal or frequent

can lead to v fib

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10
Q

v tach etiology

A
  • Usually due to ischemic heart disease and/or an acute myocardial infarction
  • Prolonged QT syndrome
  • Familial
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11
Q
* Typically presternal chest pressure radiating to the jaw and down the ulnar aspect of the 
forearm
* Typically EXERTIONAL
* Stress related
* Cold temperatures 
* Following a heavy meal

Tx too

A

Stable Angina

  • Relieved with rest, O2, nitroglycerin
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12
Q

medical tx for CAD

A
  • Treat risk factors
  • (e.g., treat HBP, elevated LDL, DM, stop smoking)
  • ASA 81 mg daily
  • Sublingual nitroglycerin
  • Beta blockers
  • Calcium channel blockers - verapamil
  • Long-acting nitrates transdermal nitroglycerin patches
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13
Q

interventional tx for CAD

A
  • PTCA/stent
  • Atherectomy
  • CABG
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14
Q
  • Progressively diminished exercise tolerance
  • Increasing frequency and severity
  • Relatively recent onset
    (unstable angina with elevated biomarkers)

tx

A

Unstable Crescendo
Non-ST elevation MI

Immediate Hospitalization
O2, nitrates, BB, Anti-thrombotic tx

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15
Q
  • Usually abrupt, severe and persistent
  • EKG
  • Biomarkers (CPK-MB; troponin-I; SGOT; LDH)

Tx

A

MI

  • 9-1-1
  • O2, nitroglycerin, and ASA to limit infarct size
  • Early intervention/reperfusion
  • tPA (tissue plasminogen activator)
  • PTCA/stent, etc.
  • Beta blockers: Acute and chronic benefit
  • ACE inhibitors/statins: Chronic benefit/plaque stabilization
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16
Q
  • Usually younger patient; at rest
  • Usually few risk factors
  • Occasional history of additional vasospastic disorders (e.g., migraine; Raynaud’s phenomenon)
  • Focal spasm of an epicardial artery with ST elevation or spasm on coronary angiography

tx

A

Prinzmetal’s Angina

  • Nitroglycerin
  • Calcium channel blockers
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17
Q
  • Asymptomatic MI
  • May present with post MI complications (e.g., CHF)
  • Frequent in diabetics
  • “Autonomic dysfunction” prevents chest pain sensation during M
A

Silent MI

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18
Q
  • Similar to angina, but not EXERTIONAL (It’s POSITIONAL)
  • Often at night (supine position)
    – Heartburn
    – Pyrosis
    – Dysphagia
  • Often relieved with nitroglycerin and antacids
  • Often midepigastric tenderness on Px
A

GERD

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19
Q

Causes of Chest Wall Pain

A
  • Usually some form of trauma/strain
    – ? Severe coughing paroxysm
    – ? Heavy lifting, etc.
  • Often pleuritic
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20
Q
  • Pain may radiate to left shoulder
  • Often relieved with sitting up and leaning forward
  • Physical exam:
    – ? Pericardial friction rub
    – ? Pulses paradoxus (decrease in BP with inspiration)
A

Pericarditis

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21
Q
  • Severe, abrupt, radiating to the back
  • Physical exam:
    – ? Loss of lower extremity pulses
    – Possible murmur of AI
A

Chest Pain Secondary to Aortic Dissection

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22
Q

Chest Pain

  • Variable and usually atypical pattern
  • Often associated with a history of anxiety and depression
  • Often precipitated by situational factors
  • Diagnosis by exclusion
A

Psychophysiological Chest Pain

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23
Q

HTN goals for blacks w/ and w/out organ damage

A

135/85 if none

130/80 is evidence

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24
Q

HTN definitions

A
  • Normal BP 120.

* Isolated systolic hypertension: Systolic BP >139, normal diastolic BP

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25
aldoseterone does what
Causes Renal Na retention to increase blood volume
26
Hypertension with not direct cause ``` Risk factors – Genetics – Sodium consumption – Obesity – Alcohol abuse – Type 2 diabetes – Type “A” personality ```
Essential HTN
27
HTN worsened with sodium consumption types and treatment
Salt Sensitive – Low renin essential hypertension • ? Excess production of unknown mineralocorticoid which does not waste potassium • Dietary sodium restriction helpful • Diuretics helpful – Normal / high renin (nonmodulating) essential hypertension • Possible renal defect (inadequate sodium excretion) • 25-30% of essential hypertension • ACE inhibitors helpful – High renin essential hypertension • Probably due to increased catecholamine activity • Beta blockers helpful • Renin blockers helpful
28
2ndry HTN causes
``` • Renal hypertension – Renovascular hypertension – Primary renal disease • Endocrine hypertension – Aldosteronism (usually primary aldosteronism) – Cushing’s disease – Pheochromocytoma – Contraceptive-induced (estrogen stimulates hepatic angiotensinogen production) – Hyper- or hypothyroidism – Hyperparathyroidism • Aortic coarctation • Obstructive sleep apnea ```
29
HTN with hypokalemia tx
Spironolactone
30
– Rapidly escalating hypertension – Borderline elevated / rising creatinine – Abrupt creatinine rise following ACE inhibitors – History of diabetes, dyslipidemia, smoking, ASCVD dx and tx
Renovascular HTN • Diagnosis – Renal artery ultrasonography; MRA; spiral CT scan – Renal artery angiography +/- renal vein renins • Treatment – Ideally, stenting
31
– Hypokalemia • ACTH; renal artery ultrasonography – Plasma aldosterone concentration and plasma renin activity levels • PAC > 20 and PAC/PRA > 30 highly suggestive – Imaging: CT/MRI
Hyperaldosteronism
32
– Symptoms usually include a severe headache, vomiting, visual disturbances, CNS findings (paresis, convulsions, lethargy, coma) cardiac decompensation and oliguria – Diastolic BP generally >130 mm of mercury, papilledema, retinal hemorrhages
Malignant HTN furosemide IV 40mg and either nitroprusside 0.25mcg/kg/mm or nitroglycerin 5mcg/min Caustion do not lower diastolic BP to
33
– No evidence of end organ damage (e.g., normal CMP or chronic abnormalities, normal UA, troponin I, no acute EKG changes, symmetrical pulses, no papilledema or retinal hemorrhages:
Severe HTN Clonidine 0.1 every 2-3h
34
– Pregnancy with hypertension, proteinuria and hyperreflexia; may present with convulsions tx
Eclampsia mg sulfate 4gIV for convulsions Hydralazine 5-10 mg IV for HTN (to d < 95) Consider urgent delivery
35
HR that compromise perfusion
Generally HR 140 compromises perfusion due to inadequate time for sufficient preload
36
Physiologic / Cardiac Compensation for CHF
Renal: – Increased sodium and water retention with renin angiotensin system activation to increase blood pressure for perfusion and to augment preload Autonomic nervous system: – Increased heart rate to increase cardiac output Cardiac: – Muscular hypertrophy – Maladaptive cellular remodeling / fibrosis
37
systolic CHF and Diastolic CHF
Systolic CHF – Primarily contractility and/or afterload problem (e.g., acute hypoxemia) Diastolic CHF – Primarily preload problem (e.g., “stiff” fibrotic ventricle) NOT to be confused with right heart failure and left heart failure
38
CHF symptoms
– Primarily dyspnea on exertion – Orthopnea / paroxysmal nocturnal dyspnea Increased pulmonary capillary pressure due to fluid shift from the extremities when supine; possible impaired apical pulmonary arteriolar oxygenation due to pulmonary effusion – Dependent edema – Cheyne-Stokes’ respirations Primarily CNS symptom likely
39
CHF physical findings
– Bibasilar inspiratory rales – Cardiomegaly / laterally displaced PMI; S3gallop – Dependent edema / pleural effusions / ascites – Hepatomegaly / positive HJR / JVP >8 cm (major criteria: >16 cm) / jaundice
40
Lab for CHF
Blood work: CBC, CMP, TSH, UA, NT pro-BNP (byproduct of stretching myocytes)
41
tx for CHF
``` Diuretics Sodium restriction BB ACEi Digoxin Vasodilators ```
42
RV failure usually due to increased RV afterload / pulmonary vascular resistance – Usually due to COPD and increased pulmonary capillary pressure from hyperinflation – Interstitial pulmonary disease / fibrosis – Pulmonary vasoconstriction (e.g., hypoxemia; altitude sickness) SOB, light head, palpitations, Chest pain, blue skin
Cor Pulmonale
43
50% mortality in 60 minutes from acute pulmonary embolism Usually due to acute pulmonary embolism – Possible high altitude pulmonary edema (HAPE); acute pulmonary inhalation injury, etc. Physical findings: – Right heart failure signs; S4 gallop tx
Acute cor pulmonale O2 diuretics, treat underlying cause
44
Pulmonary Hypertension Treatment
Treat underlying cause Oxygen Vasodilators – Calcium channel blockers; ? sildenafil (Viagra)
45
Classifications of cardiomyopathies
* Dilated * Hypertrophic * Restrictive
46
* Signs and symptoms of CHF * Usually die within three years from onset of symptoms * Rule out ischemic heart disease; work-up like CHF
Dilated Cardiomyopathy
47
* Second most common cause of CHF after ischemic heart disease * Reversible if alcohol consumption is discontinued before advanced disease * “Holiday heart syndrome” * Arrhythmias (usually AF) after a binge
Alcoholic Cardiomyopathy
48
* First symptom may be sudden death with strenuous activity (esp in kids and young adults) * May be slowly progressive and present as atrial fibrillation or CHF in older patients * Physical findings Include late systolic ejection murmur along the LLSB radiating to the apex * EKG findings LVH and often diffuse broad Q waves from increased muscle mass opposite the electrode; possible LAE; possible atrial fibrillation * Echocardiogram: Diagnostic Septal hypertrophy, left ventricular hypertrophy and systolic prolapse of the anterior mitral valve leaflet and Tx
Hypertrophic Cardiomyopathy BB or diltiazim (opposite of CHF)
49
* Diastolic CHF due to infiltrative disorders such as amyloidosis and hemachromatosis; idiopathic; familial endomyocardial fibrosis * Signs and symptoms of CHF * Treatment * Treat diastolic CHF; arrhythmias
Restrictive CM
50
* Cardiac muscle inflammation * Usually infection (e.g. viral, bacterial, lyme carditis; Chagas’ disease * Rarely autoimmune (giant cell myocarditis) * Symptoms and signs of CHF * Treatment * Treat systolic CHF, arrhythmias, underlying disorder
Myocarditis
51
from multiple etiologies (e.g., infection, acute MI, uremia, trauma / Dressler’s syndrome, metastatic disease, drugs like INH) * Symptoms * Usually chest pain referred to the back with dyspnea * Usually relieved with sitting and leaning forward * Physical findings * Pericardial friction rub; pulses paradoxus * EKG findings: Often diminished QRS amplitude and Tx
Pericarditis Treat underlying cause Pericardiocentesis: pericardial window
52
``` Opening snap rumpble augmented with exercise right CHF findings EKG: LAE Can have A fib ```
Mitral stenosis
53
• Increased left atrial pressure with symptoms of pulmonary hypertension and cor pulmonale • Regurgitated LV preload and symptoms of reduced cardiac output (e.g., dyspnea on exertion) – Physical findings • S3and occasional S4gallop • Holosystolic murmur at the apex radiating to the left axilla – EKG findings: LAE; +/- RAE; +/- LVH – Echocardiogram: Diagnostic
Mitral regurgitation
54
``` – Symptoms: • Usually none • Occasional PSVT due to LA “stretch” – Physical findings: • Midsystolic “click–murmur” augmented with isometrics and valsalva (reduced LV preload and leaflet angle with increased papillary muscle “slack”) – EKG: Usually normal – Echocardiogram: Diagnostic ```
Mitral valve prolapse * SBE prophylaxis if MR present * Beta blockers for PSVT
55
Angina Exertional Syncope (hypotension from vasodilation and exercising muscles with compromised cardiac output) Pulses parvus et tardus Reduced S1-S2 interval and possible paradoxical splitting of S2 S4 Systolic ejection murmur
Aortic stenosis
56
often asymptomatic • “Water hammer” pulse with widened pulse pressure (e.g., 140/60); “Quinke’s pulse” with gentle pressure on nail bed; markedly augmented PMI with lateral displacement (e.g., head bobbing/”bed spring” pulse) • Diastolic decrescendo murmur EKG: LVH
Aortic Regurgitation
57
SBE prophylaxis indications
– Previous history of SBE; prosthetic heart valves; prosthetic material used for cardiac valve repair; unrepaired cyanotic congenital heart disease; repaired congenital heart disease with residual defects at the site of a prosthetic device; cardiac valvular disease in a transplanted heart • Treatment prior to dental procedures: – Amoxicillin 2 gm orally one hour before procedure – Clarithromycin 500 mg one hour before procedure if penicillin allergic • Treatment prior to procedures on infected skin or musculoskeletal tissue – Infections often polymicrobial but only staph and beta hemolytic strep bacteremia are likely to cause endocarditis – Treat as above pending culture results and consider the addition of TMP SMX DS if suspicious of MRSA
58
Categories of hyperlipoproteinemia
• Type II-a hyperlipoproteinemia – Elevated cholesterol; normal triglycerides • Type II-b hyperlipoproteinemia – Elevated cholesterol; elevated triglycerides • Usually seen with type 2 diabetes
59
Acquired dyslipidemia
``` obesity Type 2 DM Hypothyroidism Liver Disease Renal Disease ```
60
Treatment goals for risk factors
0 – 2 <70
61
Risk factors for LDL elevation
``` – Cigarette smoking – Hypertension (BP 140/90 mmHg or on antihypertensive medication) – Low HDL cholesterol [<65 years – Age (men 45 years; women 55 years) – Lifestyle risk factors • Obesity (BMI 30 kg/m2) • Physical inactivity • Atherogenic diet – Emerging risk factors • Lipoprotein(a) • Homocysteine • Prothrombotic factors • Proinflammatory factors • Impaired fasting glucose • Subclinical atherogenesis ```
62
tx for elevated cholesterol
``` • Nonpharmacologic treatment – Smoking cessation – increases HDL – Weight control – decreases LDL – Exercise – increases HDL – Treatment of underlying problems such as diabetes and hypothyroidism – Dietary treatment • Low saturated fat • No dietary sweets ```
63
combo therapy for elevated cholesterol beware of what combo and why
Beware of statin/fibrate combination (myositis; rhabdomyolysis; elevated CPK)
64
meds for cholesterol and what they target
LDL only - Statin LDL, HDL, TG - Niacin TG only - Fibric acid derivatives LDL - Ezetimibe
65
Big QRS | Compensatory pause
PVC
66
PVC falls on what wave cause vent tachycardia
T wave
67
torsade de pointes (Vent fib with twisting axis) cause
Congential QT syndrome
68
Long PR consistently prolonged
1 deg AV block
69
PR interval consistently increases in successive cycles | lack of QRS
Wenkenbach 2 AV block
70
2:1 P to QRS
Mobitz 2 AV block
71
3:1 P to QRS
Mobitz 3 AV block
72
PR interval not the same | Normal QRS
3 AV block
73
bunny ears
Bundle branch block
74
Diphasic P wave
RAH or LAH
75
Large R wave in V1
RVH
76
Large S wave in V1 | Large R wave in V5
LVH
77
t wave inversion
ischemia
78
ST elevation
Injury
79
ST depression
subendocardial infarction positive stress test digitalis
80
significant q waves
infarctions
81
infarct leads
sig q waves I and AVL = Lateral V1, V2, V3, V4 = Anterior II, III, AVF = inferior
82
U waves
hypokalemia
83
A-a gradient
• Difference between alveolar O2and arterial O2 • For arterial PaO2of 80 97-80 = 17 A-a gradient of 17 • Normal A-a gradient is 7-14 on room air
84
Arterial Blood Gas Analysis PaO2: Measure of Oxygenation | Arterial Blood Gas Analysis PaCO2: Measure of
Ventilation
85
Pulmonary Function Testing | Major Types of Tests
* Spirometry (pre and post dilator) * Forced inspiratory maneuvers * Lung volumes * Diffusing capacity * Maximal respiratory pressures * Pulse oximetry – rest and exercise
86
Major Types of Pulmonary Disease Identified by PFTs
``` • Obstructive lung diseases - Asthma, COPD, CF • Restrictive lung disease - Pulmonary fibrosis, sarcoidosis, neuromuscular disease, pulmonary edema • Mixed pattern ```
87
PFTs in Obstructive Lung Disease
• Spirometry | - Low FEV1/FVC (12%) in asthma
88
PFTs in Restrictive Lung Disease
``` • Spirometry: Reduced FVC but normal or even increased FEV1/FVC ratio (>70%) • Lung volumes: Decreased total lung capacity (<80% predicted) • Diffusing capacity: Usually decreased Use of Pulse Oximetry in Clinic Setting • Measure oxygen saturation at rest • Monitor oxygen saturation . . . - With exercise - With sleep - During procedures ```
89
Hyper-responsiveness – response to triggers->Obstruction – usually fully reversible-> Symptoms – cough, wheeze, dyspnea, dec breath sounds - Airway bronchspasm - Airway inflammation and mucus • Bronchospasm - Airway narrowing - Usually worse at night - Triggers: Pollen, drugs, dust, exercise, smoke exercise, cold, stress, colds/flu
Asthma
90
Assessment of bronchospasm of Asthma
``` • Spirometry: FEV1 • Peak flow meter • Use of bronchodilators • Symptoms - Particularly nighttime awakenings ```
91
FEV1/FVC improves with dilator
Asthma
92
Signs of poor control of asthma
(rule of 2s) - Use “rescue” meds >2 times/week - Nighttime awakening due to breathing >2 times/month
93
• Defines a severe asthmatic episode that is not responsive to repeated treatments with usual inhaled medications
Status Asthmaticus
94
Treatment of Asthma
``` • Mild disease - Avoid triggers - Use of short-acting inhaler as needed • Moderate-severe disease - Inhaled corticosteroids - Inhaled long-acting bronchodilator - Leukotriene receptor antagonist Especially for aspirin sensitive asthma - Oral steroids - Anti-IgE therapy (Xolair - IgE antagonist injection every 2 weeks) ```
95
best way to improve COPD
smoking cessation
96
Low flattented diaphragm increased AP diameter Air trapping
COPD
97
Therapy in COPD
``` • Smoking Cessation • Drug Therapy --B2 agonists, anticholinergics • Oxygen Therapy • Exercise/Nutrition • Lung Volume Reduction • Lung Transplantation ```
98
``` • Respiratory manifestations - Persistent, productive cough - Airflow obstruction - Bronchiectasis-dilated airways • Physical findings - Wheezing - Clubbing of digits • Sweat chloride: Sweat chloride level of >60 meq/L - Pancreatic insufficiency with malabsorption • Infertility ```
Cystic Fibrosis
99
Restrictive lung diseases
* Interstitial Lung Disease * Neuromuscular Disease * Severe Obesity * Chest Wall/Spine Deformity * Pleural Disease
100
interstitial lung dieseases causes
``` • Drugs - Chemotherapy, amiodaronenitrofurantoin • Toxic Dusts - Asbestos, silica • Hypersensitivity Pneumonitis - Organic dusts Interstitial Lung Disease:Associated with Systemic Disease • Rheumatoid Arthritis • Scleroderma • Systemic Lupus Erythematosis Interstitial Lung Disease:Idiopathic • Sarcoidosis • Idiopathic Pulmonary Fibrosis ```
101
``` • Shortness of breath - Particularly with exercise • Cough - Usually non-productive • Radiographic - Diffuse linear (reticular) or nodular markings in lung parenchyma • PFTs - Reduced lung volumes - Reduced diffusing capacity (usually) ```
Features of ILD
102
* Military Exposure (ships/tanks) * Ship-Building * Boiler worker * Electrician * Brake Repair * Construction * Building Remodeling
ILD: Asbestos
103
* Mining * Sand-blasting * Metal working * Glass workers
ILD:Silica
104
Drug induced ILD
• Cancer patients - Many chemotherapeutic agents cause ILD, some not until years later • Cardiac patients - Amiodarone: Used for arrhythmias • Arthritis patients: Methotrexate • Urinary tract infections: Nitrofurantoin
105
Hypersensitivity Pneumonitis ILD
exposure to organic dusts | agriculture, moldy hay
106
most common cause of reduction in lung volumes, particularly total lung capacity • Diffusing Capacity (DLco) is generally not affected
Obesity and restrictive Changes in PFTs
107
``` Idiopathic Interstitial Lung Disease - Increased frequency in African-American • Clinical Presentation - Cough, Short of Breath (Lung involvement in 95% of Sarcoid pts) - Skin Rash Erythema Nodosum - Eye symptoms (iritis) - Neurologic symptoms - Joint pains -“Potato” hilar adenopathy -Facial sarcoid granulomatous nodules - “Lupus pernio” - facial sarcoid granulomatous plaque ```
Sarcoidosis
108
Sarcoid Dx
``` • Radiographic - Hilar/Mediastinal Adenopathy - Pulmonary Infiltrates • Pathologic - Granulomas: Non-caseating ```
109
• Increased prevalence in older ages • Progressive fibrosis of the lungs • Mean survival is only 3-4 years • Clinical Features - Crackles in Chest - Clubbing of Digits is Common • Exclude Other Causes of Pulmonary Fibrosis • Characteristic Features on CT: may make diagnosis Interstitial fibrosis with adjacent normal lung tissue, extensive honeycombing
Idiopathic pulmonary fibrosis
110
Treatment of ILD
``` • Known Causes - Avoid/eliminate exposure - Corticosteroids • Sarcoidosis - Corticosteroids - Methotrexate • Idiopathic Pulmonary Fibrosis - No proven therapy, ? Pirfenidone - Transplant ```
111
ARF types
• Hypoxemic Respiratory Failure - Low Oxygen Level • Hypercapnic Respiratory Failure - High Carbon Dioxide Level
112
• Acute Lung Injury: Milder injury to lung • Acute Respiratory Distress Syndrome (ARDS): Severe disorder where oxygenation is markedly abnormal (A-a gradient >200) - Approx 150,000 cases/year mortality 35-50% • Can be caused by direct injury to lung - Aspiration gastric contents - Toxic inhalation – smoke - Severe pneumonia - Exposure to drugs toxic to lungs • Systemic Injury - Shock/trauma, sepsis, drug overdose, pancreatitis, burn injury
Hypoxemic Respiratory Failure
113
Pathophysiology of Hypoxemic Respiratory Failure (ARDS)
• Alveoli fill with fluid, become unstable and collapse • Collapsed alveoli results in V = 0 which is definition of shunt • Characteristic feature of ARDS is low oxygen that does not respond to supplemental oxygen (A-a gradient >200)
114
Treatment of ARDS
• Ventilation: usually an endotracheal tube, occasionally by mask • Positive pressure throughout ventilation • Positive end-expiratory pressure (PEEP) - Supplemental oxygen - IV fluids and nutrition - Antibiotics if needed
115
Cause of death in Hypoxemic Resp failure
infectious complications
116
* May present as drop in SaO2 since increase in PaCO2 will cause decrease in PaO2 * Diagnosed by arterial blood gas demonstrating increased PaCO2 * If acute, patient will have respiratory acidosis (pH 7.2
Hypercapnic Respiratory Failure
117
some causes of hypercapnic resp failure
``` • Advanced COPD - Severe COPD Exacerbation • Severe Asthma - Status Asthmaticus • Neuromuscular Disease • Hypoventilation - Trauma, stroke, drug effect, over-sedation ```
118
most common presenting symptom of lung cancer
cough
119
syptoms of lung cancer
- cough - Hemoptysis - Wheeze, shortness of breath - Dysphagia - Weight loss - Chest discomfort - Signs of metastatic disease
120
types of lung cancer
``` • Adenocarcinoma • Squamous Cell Carcinoma • Small Cell Carcinoma (“oat cell”) • Large Cell Carcinoma • Bronchoalveolar Cell Carcinoma (BAC) type of adeno-ca that occurs as often in nonsmokers as in smokers ```
121
Staging of Lung Cancer
• Stage 1 - Small (, 3 cm) disease without involvement of any lymph nodes (N0) • Stage 2 - Larger disease, possible hilar node involvement (N1) • Stage 3 - Mediastinal lymph node involvement (N2) • Stage 4 - Metastatic disease (M)
122
Therapy of lung cancer
• For Non-small Cell Lung Cancer, surgery is the only therapy that offers a significant chance at long-term survival (>5 years) • Surgery is possible in Stage 1 disease and in selected patients with Stage 2 disease • Surgery is generally not recommended except in experimental trials in Stage 3 disease
123
Methods to stage lung cancer
CT scan | PET scan
124
ddx of lung nodule
``` • Granuloma - Usually due to fungal infection - Most often Coccidoidomycosis in Az • Lung Neoplasm - Primary or metastatic • Other unusual causes - Benign tumors including hamartoma, fibroma, etc. ```
125
what if you see a neoplasm in the airways
neoplasm (not cocci)
126
early diagnosis of lung cancer
Routine CT scans
127
lung cancer metastases sites
bone brain liver adrenal glands
128
cancer of surface of lung (pleura) often related to asbestos exposure
Mesothelioma
129
metastatic disease to lungs
Breast Colon Kidney Melanoma
130
common cold causes and tx
rhinovirus no antibiotics treat with tylenol, etcc
131
• Constitutional symptoms are more prominent than in cold - Fever, malaise, myalgias - Often seasonal • Treatable within first 2 days - Oseltamvir (Tamiflu): 75 mg bid for 5 days • Influenza prophylaxis - Oseltamvir (Tamiflu): 75 mg once daily for 6 days - Flu shots
Influenza
132
• Usually viral • 15% Strep - Exudate with fever and lymphadenopathy tx
Acute pharyngitis Penicillin or erythromycin
133
* Usually posterior cervical adenopathy, a dull white exudate and possible hepatomegaly or splenomegaly * Rash if given amoxicillin
Mononucelosis Penicillin or erythromycin
134
• Primarily results from sinus ostial obstruction (“ostiomeatal complex” obstruction) -
Acute sinusitis Narrow spectrum antibiotics Amoxicillin or Bactrim
135
sinus obstruction > 12 weeks cause
bacterial or fungal get sinus CT
136
Achy ear - Often due to pseudomonas aeruginosa and occasionally staph aureus - Generally treated with ciprofloxacin– HC drops topically and debridement; occasionally with systemic antibiotics - Avoid Q-tips
Otitis externa (Swimmer's ear)
137
usually bacterial following a viral URI - S. pneumoniae; H. influenza; M. catarrhalis - RX: amoxicillin although 1/3 resistant; treatment debatable
otitis media
138
tx for serous otitis media
- Consider antibiotics and/or myringotomy tubes if significant hearing loss and effusion > 3 mo
139
- Potentially fatal | - Dx: Lateral neck films ; cherry red epiglottis with fiberoptic rhino-laryngoscopy
acute epiglottiis ampicillin/sulbactam or 2/3 cephalosporin maybe hospitalization
140
usually viral • Characterized by cough, usually with sputum production • The absence of abnormalities on chest radiography distinguishes from pneumonia
acute bronchitis
141
severe bronchitis symptoms
- Increased amount of sputum - Change in color of sputum - Increased shortness of breath • Treat severe bronchitis with antibiotics for 7-10 days - azithromycin or levofloxacin • May need to treat associated bronchospasm (e.g., albuterol; steroids)
142
• Primary symptom is chest pain, worse with inspiration • Usually viral • Treat symptomatically - Non-steroidal anti-inflammatory drugs
Pleurisy
143
URI and LRI | What are LRIs
pneumonias
144
• Infection that extends beyond airways into pulmonary parenchyma (lobe, lobules) • Characterized by more change in gas exchange (shortness of breath), and presence of abnormal findings on chest radiograph or CT scan • Associated morbidity/mortality is much higher than bronchitis
pneumonia
145
symptoms of pnuemonia
* Cough, usually productive * Fever, chills * Dyspnea * Malaise * ? Confusion * Symptoms may vary from severe to absent
146
Physical Findings in Pneumonia
• Fever and tachycardia • Tachypnea (RR > 20) • Auscultation of chest - Common: Crackles (“rales”)
147
Types of pneumonia
• Bacteria (most often) - Gram positive: Strep pneumonia, - Gram negative: Klebsiella, pseudomonas, • Fungal - Coccidioidomycosis (Valley Fever), histoplasmosis, blastomycosis, aspergillis • Mycobacteria - Mycobacterium tuberculosis, mycobacterium avium-intracellulare • Viral - Respiratory syncytial virus, adenovirus, influenza
148
Clinical Signs of Severe Pneumonia
``` • Hypoxemia - SaO2 < 92% • Tachycardia • Hypotension • Altered mental status - Obtundation - Confusion ```
149
diagnosis of pnuemonia
• Primarily from history and physical exam • Chest x-ray / chest CT scan • Sputum Gram stain and culture - ? Acid fast bacilli stain, KOH, fungal cultures, mycobacterial cultures, etc. • Blood cultures • Serologic testing - e.g., coccidiomycosis antibody titers
150
walkling pneumonia
- Some organisms (mycoplasma or chlamydia) may cause mild symptoms
151
tx for pneumonia
• More severely ill pt, initial empiric coverage w/multiple antibiotics for a variety of pathogens - e.g., ceftriaxone 2 g IV daily with levofloxacin 750 mg orally daily • In immuno-suppressed patients, consider bronchoscopy with lavage (bronchoalveolar lavage) to evaluate for atypical pathogens • Usual outpatient treatment: Empiric macrolide (e.g., azithromycin) for mild sy mptoms or quinolone (e.g. levofloxacin) if moderate symptoms
152
• May present as community-acquired pneumonia; possible history of soil dust exposure (e.g., lives in a developing suburban subdivision) • Often causes a cavity to form within the lung • Can be associated with severe constitutional symptoms • Diagnosis: Serologic test or culturebof organisms Miliary pattern on CXR eosinophilia tx
coccidiomycosis * Most cases will resolve without any treatment * Can use Diflucan (fluconazole) 200 mg twice daily for therapy * In severe cases, may use Amphotericin B by IV administration
153
- Evidence of tuberculosis organisms multiplying in pulmonary or extra-pulmonary site - Often infectious to others
active TB
154
- Cough and minor symptoms for 2-4 weeks and central infiltrates on chest x-ray - Usually not infectious
Primary TB
155
- “reactivated” tuberculosis; symptoms may be similar to pneumonia with peripheral and apical chest x-ray infiltrates - Infectious
2ry TB
156
* Cough * Weight loss * Fatigue * Fever and night sweats * Sputum production * Hemoptysis (usually late in disease) * Dyspnea
TB symptoms
157
reactivation TB usually involves what
upper lobes | cavity will form
158
• Patients with a positive Tb skin test, but no evidence of active tuberculosis have what is termed
latent tb
159
Approach to Patient with Suspected Latent or Active Disease
• Latent disease: Tb skin testing (PPD-“purified protein derivative” or “Mantoux” testing) - mandatory in certain occupations • Suspect active disease - Isolate the patient - Sputum AFB smear and AFB culture x 3 - Occasionally will need bronchoscopy • If find active disease: Skin test all contacts
160
TB test interpretation
• Positive - ≥ 10 mm induration - ≥ 5 mm if: * HIV * Immunosuppressed * Recent close contact * Radiographic evidence of old TB
161
Latent TB tx
isoniazid 9 months with B-6
162
Active TB tx
isoniazid plus B6 Ethambutol Rifampin Pyrazinamide
163
DVT study
Duplex ultrasound
164
1. Pleuritic pain or hemoptysis 65% 2. Isolated dyspnea 22% 3. Circulatory collapse 8% No dyspnea is present 27% Tachypnea (>20) 70% Tachycardia (>100) 43% Crackles (rales) 53%
PE
165
Interventions to Reduce Risk of DVT/PE
• Early ambulation after surgery • Avoid prolonged immobilization • Compressive stocking or mechanical compressing devices • Prophylactic treatment with low-dose heparin in high-risk patients - e.g., low-dose heparin or Lovenox postoperatively then 4-6 weeks of Coumadin following a total knee arthroplasty or total hip arthroplasty
166
Diagnosis of PE
Spiral CT! (contrast enhanced) VQ scan D-dimer (sensitive to rule out)
167
Treatment of Pulmonary Embolism
``` • Initial therapy: Heparin • In unstable patient – may consider thrombolytic therapy or surgical embolectomy • Long-term therapy: Warfarin (Coumadin) - 1stepisode: 6 months of therapy - 2ndepisode: Lifelong - Predisposing factor: Lifelong ```
168
MICROCYTIC ANEMIAS
* IDA * ACD * Hemoglobinopathy (eg THAL) * Sideroblastic anemias (lead poisoning)
169
``` • Most common anemia • Most common cause: blood loss • Occasionally malabsorption from: – Gastric surgery – Malabsorptive disorders High Transferring Low serum Iron Low Ferritin ```
Iron Def Anemia dietary iron - meat oral iron
170
``` • Characterized by: – ↓Fe – ↑↑Ferritin – ↓ EPO • Develops in: – Chronic infections – Chronic inflammatory disease – Neoplastic disease ```
anemia of chronic disease
171
Macrocytic = megalo & non-megalo Name causes of megaloblastic (oval) anemias
``` • B12/Folate def • Drugs: – dilantin/OC – hydrea/methotrexate • Some marrow disorders ```
172
``` – ↑ RBC Mass – Normal O2 – Splenomegaly – Increased: WBC / PLTS / B12 / LAP score – JAK-2 Mutation – Bone Marrow Hypercellularity ```
Primary Polycythemia vera
173
polycthemia vera tx
– Phlebotomy (do it until hct under 45) • H/H < 15/45 – decreases thrombotic risk – Hydroxyurea
174
``` Anemia from reduced RBC survival (<100 days) Bone marrow unable to replace RBCs Etiologies Immune - Coomb’s Positive Non-immune - Coomb’s Negative ```
Hemolytic anemia
175
``` – Rapid pallor / anemia – Jaundice – Splenomegaly – Increase: MCV - macrocytosis • Reticulocytes – IMMUNE: (+) Direct anti-globulin test(Coomb’s) – History of pigmented(Bilirubin) gallstones ```
hemolytic anemia
176
HEMOLYTIC ANEMIA – ACQUIRED ETIOLOGIES | IMMUNE (Coomb’s +)
```  Autoimmune Hemolytic anemia(AIHA)  Warm: Idiopathic & CLL  Cold: Idiopathic & Mycoplasma  Alloimmune: Transfusion  Drug-induced ```
177
– Antibody or complement on RBC (looking for abs on RBC) – Diagnosis of: • AIHA • Hemolytic transfusion reaction
direct coombs
178
``` – ATB in SERUM NOT bound to RBC – Patient serum & Donor RBC – The screen in: “type & screen” – In autoimmune hemolysis • both DAT & IAT may be (+) • ATB may be in SERUM & ON RBC ```
indirect coombs
179
– Auto-ATB against RBCs | – Warm & Cold Auto-ATB
AIHA
180
```  Any Age  Usually IgG  Variable anemia Etiologies:  65% - Idiopathic  25% - CLL  20% - NHL  Other – Meds Clinical  Anemia  Jaundice  Splenomegaly ```
warm auto ATB
181
``` – IgM – Etiologies: • Idiopathic • Mycoplasma • Lymphoma • Mononucleosis – Clinical • Acrocyanosis at cold temperatures • Jaundice • Splenomegaly ```
cold auto atb
182
acquired clonal stem cell disease – Cell membrane anchor defect – Hemolytic anemia – Screen using: CD55 and CD59 and treatment
Paroxysmal Nocturnal Hemoglobinuria Elulizumab -binds complement C5
183
Inherited hemolytic blood disease resulting from a mutation in the alpha globin gene • Normal HGB = “A1” • Hemoglobin “S”
Sickle Cell Disease
184
Sickle Cell Types
``` – “Trait” = Heterozygous = A>S • 8% of Aas • Malaria protection – “Anemia” = Homozygous = SS • sickle cells in PS – Sickle cell – Hemoglobin C = “SC” • fewer sickle cells - more Target / Spherocytes – Sickle-Thal ```
185
Vaso-occlusive disease of sickle cell
– SC accumulate in any vascular bed – Infarction of Marrow/Spleen/Kidney – Painful crises in long bones • MOST COMMON PRESENTATION
186
sickle cell skeletal presentation
* Marrow hyperplasia=osteopenia=fractures * “Hair-on-end” on skull * Marrow infarction = osteonecrosis * Dactylitis * Osteonecrosis * Bossing
187
``` – 8% of African Americans – A always > S – Under physiologic conditions no vaso-occlusion – Carriers have normal life expectancy – Compared to the general population: • Same risk for: – Heart disease – Stroke – Anesthetic agents ```
sickle cell trait
188
``` – Imbalanced globin chain synthesis: • Ineffective hematopoiesis • Defective Hgb production • Hemolysis • Variable anemia ``` types and explian
``` • Beta Thalassemia – Beta reduce or absent – Alpha excess • Alpha Thalassemia – Alpha reduced or absent – Beta excess • Quantitative NOT Qualitative disorder ```
189
heinz bodies
excess alpha chains
190
``` – Heterozygous carrier – Usually no clinical symptoms – Asymptomatic Splenomegaly 20% – CBC/peripheral smear • Mild anemia(Hct>30) • MCV ```
B-Thal Minor
191
``` • Anemia later and milder than major • Requires less transfusion • Retarded growth/development • Skeletal deformity – EPO increases marrow expansion – Deformities of skull / long bones – Pathologic fractures • Splenomegaly • Milder forms: – Asymptomatic & xfusion independent – Hgb 10-12 ```
B thal Intermedia
192
``` • Homozygous “Cooley’s Anemia” • Symptoms begin at 4-6 months • Clinical: – Gallstones – Leg ulcers – Skeletal disease – Anemia Laboratory features • Microcytic anemia • Target cells / Tear drop cells / Basophilic stippling / NRBCs ```
B thal Major
193
Pathophysiology Alpha Thalassemia
``` – 4 copies of α globin gene • 2 copies each Chr. 16 – 1 Deletion = AT Minima – 2 Deletions = AT minor • TRANS: A/- A/-• CIS: AA / --– 3 Deletions = Hgb H Disease – 4 Deletions = Hgb Bart’s ```
194
``` – Silent carrier = (α - / α α) – Trait • Similar to β Thal trait • Mild heme changes • No clinical abnormality ```
a Thal (silent carrier)
195
* Mod-severe hemolytic anemia – hypo/micro –retic counts to 15% * HSM / Gallstones / Leg ulcers * RBCs contain Hgb H precipitates
– Hgb H Disease (α - / - -)
196
– Hgb Bart’s (- - / - -) (γ4) =
incompatible with life
197
other names for myelodysplastic syndromes
– Refractory anemia • No improvement with Fe / B12 / Folate – Pre-Leukemia – Senile anemia
198
Ringed sideroblasts
myelodysplasia
199
``` • Heritable mutation = RUNX-1 • Tobacco • Ionizing Radiation – Highest rate of progression to AL – 75% – Low response to treatment – Median survival ~ 9 MOS. – Chromosome abnormalities: • -5 / -7 = Alkylating Agents • 11 = Topo-II inhibitors Clinical: – Signs / symptoms usually from cytopenias • Anemia • Infection • Bleeding – Usually absent: • Lymphadenopathy • Hepatosplenomegaly Peripheral smear: • Macrocytosis • Hypolobar neutrophils – (Pseudo Pelger-Huet) • Circulating micromegakaryocytes ```
Myelodysplasia
200
myelodysplasia therapies
Bone Marrow Transplant is only curative
201
``` – van den Berghe Nature 1974 – severe anemia – mild leukopenia – normal or increased platelets – atypical megakaryocytes – indolent – <5% blasts ``` 5q treatment
5q syndrome Lenalidomide
202
Myeloproliferative Disorders
• BCR/ABL(+): Chronic Myelocytic Leukemia • BCR/ABL(-) & JAK2(+): – Essential Thrombocythemia – Myelofibrosis with Myeloid Metaplasia – Polycythemia rubra vera • JAK2(+/-): Chronic Myelomonocytic Leukemia
203
``` • 10% of all leukemias • Adults>>>children • Median age = 50 • M>F • IR only known causative factor (Ionizing Radiation) MPD - CML • BCR/ABL • “Philadelphia Chromosome” Basophilia – Fatigue / weight loss / night sweats – Splenomegaly – Leukostasis from Hyperleukosis 3 phases (Chronic, accelerated, blastic - acute leukemic transformation) ```
CML
204
CML treatment
Imatinib (Gleevec)
205
``` •Most common MPD •Age at diagnosis: 50-60 JAK + Bone Marrow = increased MEGS •Near-normal life expectancy – PLTS > 600K – Microvascular Thrombi – Bleeding – Splenomegaly – Recurrent first trimester abortions – Leukemic transformation very low ```
Essential Thrombocytopenia
206
• 33% asymptomatic at diagnosis • Fatigue / Weight loss / Fever / Night sweats • Anemia • Splenomegaly – Leukoerythroblastosis – Single or multiple cytopenias • Bone marrow - fibrosis - “Dry tap” – Fibrous tissue takes place of normal BM tissue • Leukemic transformation in 20% during first decade
MYELOFIBROSIS WITH MYELOID METAPLASIA
207
``` • Affects all 3 cell lines - RBCs the most • Proliferate without EPO • Serum EPO levels are low • Median age = 60 • Increased HGB/HCT/RBC mass • Bone marrow: Hypercellular • B12 increased from increased WBCs producing B12-binding protein • Symptoms related to increased viscosity – Plethora – Erythromelalgia – Pruritus • Arterial/Venous Thrombosis • Thromboses: » Renal/portal veins » Budd-Chiari » Mesentery ```
Polycthemia Rubra Vera
208
– Most common neoplasm in
ALL
209
ALL sites
Marrow usually
210
ALL presentation
– Bulky adenopathy – Mediastinal mass – Pleural effusions – +/- hyperleukocytosis
211
ALL Lab
– ↑ WBC or Pancytopenia +/- Blasts – LDH (= tumor burden) – Hypercalcemia – ↑ Uric acid / LFTs / BUN
212
ALL treatment phases
– Induction – CNS – Consolidation – Maintenance
213
``` • Uncontrolled prolifeation of myeloid progenitors • Replaced hematopoietic elements • Ineffective hematopoiesis • Majority de novo • Treatment related – Chemotherapy: CHR: -5 / -7 / 11 – RT Auer Rods ```
``` – Bone marrow failure – Abnormal hemostasis • Thrombocytopenia • Coagulopathy • DIC most common with APL ```
214
``` • Lymphoid Neoplasm • Binucleate giant Reed-Sternberg cell • 75% of pts can be cured • Origin – Germinal B Center lineage • Other adenopathies – Mononucleosis -EBV ```
Hodgkin's Lymphoma
215
Hodgkin's Lymphoma clinical features
``` – Adenopathy • 80% Cervical • 50% mediastinal • Nontender / firm-pliable – B symptoms • Fever • Night sweats • Weight loss – Other symptoms • Fatigue • Weakness • Anorexia • Etoh induced node pain • Pruritus ```
216
review difference between B cells and T cells
``` • B cell – Produced and mature in marrow – B cell receptor – Antibody production – Plasma cells • T cell – Produced in marrow – Mature in Thymus – T cell receptor – CD4: Helper T cells – CD8: Cytotoxic T cells ```
217
t(2;5) t(8;14) t(14;18) t(11;14)
ALCL Burkitts Follicular Mantle
218
``` – Family History – Previous neoplasm – Immune suppression – Infection – “B” symptoms – Weight loss: >10% weight in 6 months – Fever – Night sweats • Physical examination – All node bearing regions including Waldeyer’s – Organomegaly – Skin involvement ```
NonHodgkins Lymphoma
219
Non Hodgkins types
* INDOLENT * Chronic Lymphocytic Leukemia * Follicular Grade 1/2 * MALT * Lymphoplasmacytic Lymphoma * AGGRESSIVE * Follicular Grade 3 * Diffuse Large Cell * Anaplastic Lymphoma * Mantle Cell Lymphoma * Primary CNS Lymphoma * Acute Lymphoblastic Lymphoma
220
``` • Median seventh decade • BM-PB-LN/L/S • SLL = tissue equivalent of CLL • Incurable/median survival ~ 10 YRS • Can transform to: – Prolymphocytic leukemia – Large B Cell lymphoma (Richter’s) • Treatment • Oral agents - Chlorambucil • IV/Biologics - Rituximab ```
CLL
221
``` • Also called Waldenstrom’s macroglobulinemia • median seventh decade • BM/LN/S • Rarely – PB / extranodal • IgM elevated Very high = hyperviscosity • Generally incurable • MS ~ 9 YRS ```
Lymphoplasmacytoid Lymphoma
222
``` • Median sixth decade • 35% of NHL • BM/LN/S/Extranodal • May transform to aggressive • Early stage - therapy • Advanced stage not curable – Initial treatment may be surveillance t14:18 ```
Follicular Grade 1 or 2
223
* Median seventh decade * Three subtypes: MALT/Nodal/Splenic * Can be nodal or extranodal * Extranodal often with Autoimmune disease * Sjogren’s * Hashimoto’s * H.pylori gastritis * Incurable – MS ~ 10 YRS. * Early MALT treat with antibiotics
Marginal Zone
224
* Median seventh decade * M>>F * t(11;14) * Increased Cyclin D1 * BM/LN/Extranodal sites * Lymphomatous polyposis * Incurable * Shorter MS – 3-5 YRS
Mantle Cell
225
``` • 30% of lymphomas • Median age sixth decade • Extranodal in 40% • Curable with chemotherapy – Most with early stage – 50% with advanced • CNS prophylaxis occasional ```
Diffuse Large B cell lymphoma
226
``` • Most common Pediatric NHL • African = “Endemic” Form = EBV + • Western – Adults – Sporadic – EBV -– Mesenteric LN – Ileum – Cecum – Liver - Spleen • Curable with aggressive therapy • CNS prophylaxis required t8:14 ```
Burkitts
227
``` – Cutaneous & systemic – Systemic form • children & adults • Expresses t(2;5) • Mainly T cell – Cutaneous • Mostly adults • Isolated skin nodules • Is more indolent and incurable ```
Anaplastic Large Cell
228
* Cutaneous T Cell lymphoma * Multiple cutaneous plaques – nodules * Generalized erythroderma * Treatment often topical
Mycosis Fungoides
229
``` • In HTLV-1 areas: – Japan – Carribean • Presentation: – High WBC – HSM – Hypercalcemia – Lytic bone lesions • CD-30+ = Ki-1 • t(2;5) • Four clinical presentations: – Smoldering – Chronic – Lymphomatous – Acute ```
Adult T cell Leukemia/Lymphoma
230
* Incidence 60x greater than general population * Median age fourth decade * Usually ST III/IV * Often extranodal: GI/BM/CNS * Primary CNS lymphoma common in this group * 70% = large B Cell / other = Burkitt-like
Lymphoma HIV associated`
231
Typles of plasma cell neoplasms
``` • Clinically Benign: – MGUS • Indolent: – Waldenstrom’s – Indolent Myeloma • Malignant: Plasma Cell Myeloma • Malignant Aggressive: Plasma Cell Leukemia ```
232
``` • Definition: – M Protein(G,A,M)Value < 3.0 g/dl – No Urinary Light Chains – Normal • CBC • Renal function • Calcium • Bone – Bone marrow plasmacytosis < 10% ```
MGUS
233
1. Monoclonal protein serum a/o urine 2a. Plasmacytoma OR 2b. Marrow plasmacytosis > 10% 3. CRAB: • Calcium • Renal - light chain tub interst nephritis • Anemia • Bone - osteoporosis Rouleax formation
Multiple Myeloma
234
Myleoma symptoms
``` back pain headache blurry vision CHF Sausage retinal veins ```
235
Collection of plasma cells usually in vertebral body
Solitary Plasmacytoma (treat with bisphosphonates)
236
virchows triad
– Venous stasis – Blood vessel damage – Hypercoagulability
237
Disorders of Thrombosis -Prophylaxis in Podiatric Surgery | 3 significant risk factors
– Prior VTE – Hormone replacement/Oral Contraception – Obesity
238
``` – Most common heritable risk factor – Factor V resists lysis by Prot C – Caucasians: 5% incidence • Majority = no thrombosis – 20% with VTE + – VTE risk increased by other risk factors ```
Activate Protein C Resistance
239
* Increase O2 carrying capacity * Not for volume replacement * Symptomatic anemia / acute hemorrhage * Increase HGB in adult ~ 1 GM / DL
Packed RBCs
240
* Replaces volume and O2 carrying capacity * <1% of all xfusions * Large amount of plasma
Whole Blood
241
* Wash with saline to remove plasma | * Indication – repeated hypersensitivity reactions
Washed RBCs
242
* Remove WBCs by filtration | * Indication – multiple non-Hemolytic transfusion reactions
Leukoreduced RBCs
243
``` – From whole blood – Preserves labile proteins except Factors V & VIII – Efficacy limited by: • Shortest ½ life of factor being replaced(Often Factor VII) • Degree of factor deficiency – ABO compatible – Indications: • Replace coagulation factors • Factor deficiencies – With bleeding – Scheduled for surgery • DIC • Liver disease • Rapid reversal of warfarin ```
Fresh Frozen Plasm
244
``` – Cold soluble proteins left when FFP is thawed. • FVIII / FXIII / Fibrinogen • vonWillebrand’s Factor – Replacement of Fibrinogen – ABO not needed – Indications: • Deficiencies: – Fibrinogen – F XIII • DIC • Hemophilia A or vWD (when no FVIII concentrate) ```
Cryoprecipitate
245
``` • Diagnosis of exclusion • Common: – 1% of RBC – Up to 30 % of PLT xfusions • inc temp. ≥ 1 deg F near end or following • Recipient ATB vs. Donor leukocyte ATG • Symptoms: – Hallmark is fever – Chills / Hypertension / Tachycardia • Usually transient ```
Febrile Nonhemolytic Transfusion Reaction
246
``` – Most=ABO incompatible • Often mislabeling or wrong ID – 1:25,000 – Mortality 17-60% – Fever/chills/dyspnea/chest pain – Shock-death – Hallmark = Intravascular hemolysis: • Complement fixation by IgM • Hemoglobinemia - Hemoglobinuria – Direct Coomb’s = + – Indirect Bili – Jaundice – ATN ```
Acute hemolytic transfusion reaction(immune
247
``` • Rapid extravascular clearance of xfused RBCs – Immunized prior xfusion(“primary”) – Days or weeks • May be mild and unnoticed • More common than acute: 1:7000 • Hallmark = unexplained decrease in Hgb • Fever / chills • Lab: – Increase Bili / LDH / reticulocyte count – Jaundice – DAT usually + – Decrease in Haptoglobin ```
Delayed Hemolytic Transfusion Reaction
248
``` • Small amount • Sudden onset & rapid progression – Respiratory distress – Vascular collapse – Afebrile • IgE response to transfused proteins • Particularly susceptible IgA deficients ```
Anaphylactic Reaction
249
* Noncardiogenic pulmonary edema * Usually ~ 2 hours after xfusion * Acute respiratory insufficiency & hypotension * CXR = bilateral white out * Fatality 7%
TRALI
250
Platelets are involved in _________ hemostasis
primary
251
How does thrombocytopenia present
– SPONTANEOUS BLEEDING – PERSISTENT BLEEDING – EASY BRUISABILITY(WITH OR WITHOUT TRAUMA) – OOZING OF BLOOD - OFTEN FROM MUCOUS MEMBRANES – UNEXPLAINED GI OR GU TRACT BLEEDING – UNEXPLAINED RED FLAT PINPOINT RASH - OFTEN LOWER EXTREMITIES
252
- Intravascular purpura - Platelet disorders - <3mm - Non-palpable
Petachia
253
thrombocytopenia bone marrow smear
increased cellularity | megakaryocytes
254
* Most common cause of easy bruising in a healthy adult * Females > Males * Decades 2 & 3 * Easy Bruising * Diagnosis of exclusion * Bone Marrow = Megakaryocytes OK * No Splenomegaly * Rx:Prednisone/Splenectomy/IVIG/Neumega/Romiplostim/Eltrombopag
Immune Thrombocytic Purpura
255
``` – dec Platelets and fibrinogen – inc FDP - PT - PTT - Thrombin Time – inc D-Dimer: • degradation of stabilized fibrin • confirms thrombin generation & FXIII cross-linking Non-immune get Schistocytes – thrombosis - smaller vessels – bleeding = Factor Consumption & Plasminolysis – treat etiology ```
DIC | Diffuse Intravascular Coagulopathy
256
``` • Large vWF multimers – Lack protease • Thrombi: CNS - Kidneys - Myocardium • Peak = 20s F = 65% • Clinical: – Fever – MAHA - Thrombocytopenia – Neurologic - Renal – Hematuria – Proteinuria – Schistocytes - NRBCs – Normal: PT/PTT/fibrinogen ```
TTP
257
* Children>Adults * Prior Infection * vWF protease normal * MAHA / Thrombocytopenia (< TTP) * ARF (renal > TTP) * No Neurologic or Fever
HUS
258
Platelet Transfusion - Parameters
– 60,000
259
Definitions of Hemostasis
* Primary: Platelet Plug: * Platelets + vascular injury = platelet plug * Requires VWF + FVIII * Activates secondary * Secondary: Fibrin Plug: * Activation of the coagulation cascade = fibrin plug
260
Disorders of Hemostasis - Coagulation Cascade
``` • Extrinsic (Checked with PT/INR) – Tissue Factor + FVIIa – Converts X -> Xa – PT/INR • Intrinsic • Initial sequence – Vascular injury – Kallikrein activates F XII – Cascade follows • aPTT ```
261
– Prolongation: dec in Fs II/V/VII/X/Fibrinogen – Extrinsic system abnormalities – INR(Int. Normalized Ratio) for Warfarin patients
Prothrombin Time(PT
262
Prolongation is dec for factors II/V/VIII/IX/X/XI/XII – Intrinsic system – Rarely affected by fibrinogen
aPTT
263
Disorders of Hemostasis - Mixing Studies
– Prolonged PT / aPTT from deficiency? – Mix patient and control plasma – Correction • qualitative or quantitave factor abnormal – Noncorrection = factor inhibitor • Lupus anticoagulant (Mix w/normal control. If PTT is corrected it means there is a deficiency (Present with bleed, bruise) If it doesn’t correct then SLE (these will present with thrombosis)
264
Abnormal PT
``` – Vitamin K deficiency • Vitamin K dependent factors measured by PT = II/VII/X – Coagulopathy of liver disease • Initial = Decreased F II/VII/X • Factor V – NOT Vitamin K dependent. – Hepatic disease vs. other prolonged PT ```
265
abnormal aPTT
``` – Hemophilia • A = congenital def of F VIII • B = congenital def of F IX – von Willebrand’s disease • dec vWBF = dec FVIII = inc aPTT • Corrects on mixing – F XII Deficiency – LA • no correction with mixing ```
266
Abnormal PT + aPTT
``` – Coagulopathy of liver disease – Deficiencies of individual factors • Factor II (Prothrombin) • Factor X (Stuart-Prower) • Factor V (Proaccelerin) – DIC – LA ```
267
cuases of ataxic gait
posterior column disease cerebellar degeneration peripheral neruopathy
268
Steppage gait causs
LMN disease such as neuropathies (syphillis) Tabes dorsalis
269
Stiff spinal cord gait - circumduction gait
UMN disease
270
Magnetic gait
Normal Pressure Hydrocephalus
271
glasgow coma scale
``` Eye Spon 4 resp to speech 3 resp ot pain 2 No respons 1 ``` ``` Motor Obeys 6 Localizes 5 Withdraw 4 abn flxr 3 abn ext 2 no response 1 ``` ``` verbal oriented 5 confused 4 inappropriate 3 incomprehensible 2 no response 1 ``` 15 = wnl, < 8 fatal, 3 = dead
272
``` Resting tremor unilateral cogwheel rigidity Bradykinesia asymmetric onset treatment ```
Parkinsons disease start with levodop or dop agonist first to control symptoms
273
``` Less tremor than parkinsons vertical gaze impaired Stiff gait --Fall backward Axial rigidity, hyperextended Falling is big concern ```
Progressive supranuclear palsy
274
An action tremor with a high amplitude and high-frequency. Tremor kicks in when you use your hands for example Bilateral, postural and action tremor Duration > 3 years Family history Alcohol response – worse with alcohol Otherwise neurologically normal
Essential tremor treatment mysoline and BB
275
Usually occurs in young people (mean is 29 years) Optic neuritis (Loss of vision, double vision, Internuclear Opthalmopelgia) Vertigo/Diszziness & Insomnia, Oropharyngeal problems – dysphagia, slurred speech Demyelinating lesions are found in the brain and spinal cord Deep white matter plaques Test to order
Multiple Sclerosis cranial MRI with Gadolinium
276
Types of MS
Relapsing – Remitting (RRMS) Seconary progression (SPMS) RRMS with multiple increasingly frequent relapses Primary Progressive MS (PPMS) Clinically Isolated Syndromes suggesting MS (CIS) Isolated single episode Benign MS 15% don’t relapse 15% may have plaques at autopsy with no history of MS
277
acute flares of MS treated with
IV glucocortricoids
278
ACh Receptor Antibodies 10 to 15% of MG patients have thymoma (benign) Fatiguibility that IMPROVES with rest Ptosis – usually bilateral, but may be unilateral Diplopia Fluctuating weakness Testing includes: Tensilon tests, EMG/NCV, Chest CT, ACh Receptor antibodies Repetitive stimulation -> NCV decrement – due to ACh depletion
Myasthenia Gravis Mestinon, Immunosuppressant Avoid NM blocking drugs
279
Antibodies against voltage gated calcium channels – impairs Ach release Almost all are > 40 y/o Most are paraneoplastic in nature Think Cancer! -> Small cell of lung, Lymphoproliferative disorder, pancreatic cancer, ovarian cancer, Breast cancer LEMS precede cancer by 1 year Looks just like MG Proximal weakness (LE > UE) Easy fatigubility Strength and DTRs may improve after isotonic exercise Dysautonomia more common than MG -> especially dry mouth! EMG/NCV Increment on NCV after repeat stimulation (not decrement) Treat by finding cancer and treating that
Lambert Eaton Myasthenic Syndrome
280
UMN and LMN disease; CNS & PNS Loss of Motor neurons in corticospinal tract Eventually may get frontal lobe dementia Hyperreflexia, Atrophy, Fasciculation, Weakness, Spastic, Painless usually Skeletal muscles -> eventually diaphragm EOM only muscles spared Pure motor disease Above levels also affected Dx via EMG!! – not NCV Supportive Care; Riluzole may prolong life expectancy by 3 months
ALS
281
Can be Compressive myelopathy Motor and sensory symptoms Below level affected
Spinal stenosis
282
Meylopathy "Cape-like numbness", Symptoms of myelopathy include paraparesis and a sensory level Intraxial widening of the central canal
Syringomyelia
283
Pathology of the spinal cord
myelopathy
284
myelopathy signs and symptoms
``` Spasticity Upper motor neuron Sensory level Bladder and bowel incontinence Pain Characteristic gait: Stiff and erect (Stiff Man Gait) ```
285
A febrile diabetic with back pain and myelopathy has what?
epidural abscess til proven otherwise
286
Acute; (+) Straight leg test Front of leg = L3/L4; Lateral = L5; Radiates to heel = S1 Sensory & reflex changes usually immediate w/ onset of pain
sciatica
287
Confused w/ cellulitis & DVT Usually post-op  Severe hypersensitivity w/ swelling & sweating
CRPS/RSD/Causalgia
288
``` Desire to move legs Feeling of motor restlessness Worse with rest or at night Better with activity dx by history ```
Restless leg syndrome
289
Drugs taht cause tremor
beta agonists (sympathomimetics) Lithium Antipsychotic Valproic Acid
290
Drugs associated with PerNeur
amidoraone vincristine metrnidazole halothane Vincristine B-6 INH are the biggies
291
drugs with myopathis
statins steroids accutane chloroquine
292
General myopathy symptoms
``` Painful Myalgias Cramps Contractures Myotonia - Stiff Myoglobinuria No weakness, fatigue, exercise intolerance, muscle atrophy ```
293
``` Boys Absent dystrophin Pseudohypertrophy Positive Gowers sign Cognitive imparitment Waddling gait Cardiac probs High CPK ```
Duchenne's
294
myopathies vs NMJ
NMJ Diseases generally involves proximal muscular weakness and is symmetrical. See MG and LEMS above
295
Endocarditis or arrhythmia associate with what stroke
embolic
296
HTN with what stroke
Lacunar
297
CAD with what stroke
thrombotic
298
Collective term that refers to different types of motor behaviors that are present in patients who have lesions of the descending corticospinal system
Spasticity always think brain or spinal cord
299
common causes of spasticity
``` Stroke Cerebral Palsy Traumatic brain injury Anoxia Spinal cord injury MS ALS, PLS, MSA Metabolic diseases (Leukodystrophies) ```
300
treatments for spasticity
``` Benzodiazepines, Baclofen, Tizanadine (Zanaflex) Botox. Also PT, serial casting, orthoses, orthopedic procedures ```
301
``` Unilateral pulsating moderate to severe aggrevated by activity Photo & or phonophobia prodrome -> aura -> HA -> post drome ```
migraine
302
types of migraine
common - no aura classic - aura complex - focal neuro deficity basilar - HA, N, vertigo
303
tx for migraine
non pharm - foods, etoh, caff acute - nsaids, ergot, steroids, narcotics preventative - TCA, CCB (2nd) BB, Depakote, botox
304
``` Unilateral severe ice pick retroorbital stiffness, rhinorrhea, occur in clusters smoker ```
cluster 02, steroids, lithium CCB
305
``` base of skull to temporal region band like palpable muscle tension stress overlap with migrain 30 min to 7 days pressing or tightening ```
tension
306
worst HA of my life
sub-arachnoid hemorrhage neuro emergency
307
``` parkinsonisms frontal visuospatial dementia fluctuating cognition recurrent visual hallucination lang and mem still good ```
Lewy body dementia
308
magnentic gait | incontinenc
normal p hydrocephalus
309
How are peripheral neuropathies classified?
``` Acute Chronic Motor Sensory Compression Hereditary Axonal – Lower Amplitude Demyelinating – Slower amplitude ```
310
myelinopathies types
acute - guillian barre | chronic
311
Antibodies cross react with antigens on Schwann cells Associated with infections above Progression over course of 2 to 4 weeks with nadir by 2 weeks If longer than 8 weeks think CIDP Ascending symmetric weakness* DTRs absent* Tingling dysesthesia EMG/NCV shoe conduction block or prolonged motor velocities CSF shows elevated protein and pleocytosis of 10 lymphocytes Treatment is Plasma exchange or IVIG within 7 days of onset
guillan barrre
312
NM disease DTR intact Perioral numbness dysphagia
botulism
313
rule of 9's for glial based tumors
grade 4 - GBM - 9 mo to live grade 3 - astrocytoma - 18 mo to live grade 2 - glioma - 27+ mon
314
Signs and symptoms of osteoporotic fracture
height loss, kyphosis, or unexplained back pain | previous or current facture
315
mechanism of bisphonsphonates
*1. Inhibition of osteoclast formation *2. Inhibition of osteoclast activation *3. Inhibitation of mature osteoclast activity *4 Reduction in osteoclast life span-apoptosis Can cause Jaw osteonecrosis & frozen bone
316
PTH analog
Teriparatide
317
Actions of cortisol
• Primary active glucocorticoid • Antagonizes insulin secretion and action • Stimulates gluconeogenesis • Impairs protein synthesis in bone, skin, muscle and connective tissue • Impairs macrophage production of inflammatory cytokines • < 5% cortisol is free, physiologically active, and still filterable by the kidney • Circadian cycle – Peak before waking; nadir before sleeping
318
Actions of aldosterone
• Primary mineralocorticoid • Stimulates Na+ / K+ sodium pump in the renal collecting duct – Minor Na+ retaining actions also on salivary ducts, sweat glands and GI tract
319
actions of androgens
• DHEA and androstenedione are produced mainly in the Z. reticularis – Weak androgens, but converted to testosterone (a more potent androgen) in the testes • In males, adrenal androgens of little significance • In females, adrenal androgens are the major source of androgens and responsible for the development of pubic and axillary hair and for libido
320
Stimulation testing
• For adrenal cortical insufficiency • ACTH (cosyntropin) stimulation test – IV ACTH stimulates an appropriate cortisol response in normals • Furosemide stimulation test – IV furosemide then 3 hours upright stimulates an appropriate aldosterone response in normals • Metyrapone stimulation test ( for secondary adrenal cortical insufficiency) – Oral metyrapone impairs cortisol production resulting in an appropriate ACTH rise in normals
321
Suppression Testing
• For adrenal cortical hyperfunction • Dexamethasone suppression test – 1 mg of dexamethasone orally at midnight lowers 8 AM plasma cortisol level in normals • Saline suppression testing – Normal saline at 500 cc/hr for 4 hours lowers serum aldosterone level in normals
322
– Muscle weakness; fatigue; weight gain; possible diabetic symptoms; menstrual changes; emotional changes; skin changes • Signs – Cushingoid facies; centripetal obesity; “buffalo hump”; edema; abdominal stria; hirsutism; HBP; osteoporosis
Cushing's Syndrome Iatrogenic most common
323
Cushing’s Diagnosis
– Elevated plasma cortisol – Dexamethasone suppression test failure – ACTH may be elevated or low
324
Cushing’s Treatment
– Pituitary or adrenal surgery • Adrenalectomy with replacement therapy conveys a 10% risk of a pituitary tumor w/in 10 years – Steroidogenesis inhibitors (e.g., ketoconazole, mitotane) • Generally reserved for poor surgical candidates
325
adrenal adenomas are common | t/f
true
326
• Usually 2° to an adrenal adenoma – possibly 2° to cortical nodular hyperplasia • Generally presents as hypertension with hypokalemia – Possibly accounts for up to 5% of hypertensive patients – Usually no edema 2° to “escape phenomenon” • Diagnosis – Elevated aldosterone levels • Plasma aldosterone concentration (PAC) and plasma renin (PRC) concentration: – PAC / PRC > 30 highly suggestive – Failure to suppress aldosterone with normal saline suppression testing
Primary aldosteronism (Conns syndrome)
327
Secondary aldosteronism
• Usually renovascular disease (e.g., renal artery stenosis) – Rare renin producing tumors (e.g. juxtaglomerular cell tumor) • Edematous conditions (e.g., cirrhosis; nephrotic syndrome; CHF) – “third space” fluid but arterial hypovolemia prompts aldosterone release
328
• Symptoms and signs – Fatigue; weight loss; nausea and vomiting; “bronze hyperpigmentation”; hypotension • Diagnosis – Low serum cortisol; elevated ACTH – Hyponatremia with hyperkalemia – Inadequate cortisol response to ACTH stimulation test
Primary adrenocortical insufficiency | Addison's Disease
329
treatment for addisons
– Hydrocortisone 20-30 mg daily | – Fludrocortisone 0.05-0.1-mg daily
330
• Possible panhypopituitarism • Generally iatrogenic – Rapid withdrawal from long-term steroid therapy • Especially fluorinated steroids – Medications (e.g., Dilantin, ketoconazole, rifampin, mitotane) • Alternate day prednisone to preserve HPA axis – e.g., prednisone 20 mg every other day; tapering from 10 mg of prednisone daily to 10 mg and 5 mg on alternate days, then 10 mg every other day, etc.
2ry adrenocortical insufficiency
331
• Hypovolemic cardiovascular collapse | – Fatal if unrecognized
addisonian crisis
332
addisonian crisis tx and prevention
• Treatment – IV Hydrocortisone 100-mg bolus followed by 10 mg / hour continuous infusion • Prophylactic stress steroids – 75-100 mg of hydrocortisone daily – Hydrocortisone 100 mg IV preoperatively
333
``` – Symptoms • Paroxysmal beta adrenergic symptoms – Laboratory findings • Urinary free catecholamines, VMA, metanephrines – CT scan tumor localization ```
Pheochromocytoma
334
treatment for pheochromocytoma
phenoxybenzamine
335
type 1 DM clinical manifestations
``` polydipsia polyuria polyphagia Ketosis-prone absolute insulin deficiency ```
336
infants and children first manifestation of Type 1 DM
ketoacidosis
337
type 2 clinical manifestation of type 2
``` recurrent infections genital pruritis hyperglycemia, visual changes parasthesias and fatigue ```
338
effects of hyperglycemia
glycation of proteins (hemoglobin, collagen) accumulation of sorbitol and fructose (nerves, lens) activation of protein kinase C (vascular cells)
339
Diagnositc criteria for DM
 Hemoglobin A1c 6.5,  FBS 126,  2 hour postprandial glucose 200  Diagnostic criteria for IFG (FBS 100-125);  Diagnostic criteria for IGT (2-hour postprandial glucose 140-199);  Hemoglobin A1c 6.0-6.5 "high risk" for diabetes
340
type 1 general treatment
insulin lifestyle modification --no glycemic control
341
General treatment of type 2
diet, exercise, drugs | Glycemic control
342
 Mechanism of action: Decrease hepatic glucose production  Little risk of hypoglycemia;  Lactic acidosis with CHF and renal failure;  Weight neutral Insulin secretagogues:
metformin
343
insulin secretagogues names
sulfonylureas (glyburide, glipizide) repaglinide nateglinide
344
 Mechanism of action: Increase basal and/or postprandial insulin secretion  Hypoglycemia can happen  Weight gain can happen
Sulfonylureas/glyburide:
345
Possibly useful before the heaviest meal of the day
Meglitinides/nateglinide
346
 Suppresses appetite;  Weight loss;  Improved insulin sensitivity;  Injectable
GLP-1 agonists/Exanatide:
347
 Oral; similar to GLP-1 agonists but weight neutral
DPP-4 inhibitors/sitagliptin:
348
 Mechanism of action: Enhance tissue response to insulin  Weight gain  CHF risk  long bone fracture risk
TZDs/pioglitazone:
349
generally start type 2 DM meds with what
metformin and/or a sulfonylurea
350
insulins - short, normal and long acting
``` aspart, glulisine, lispro - 4-6 hrs regular - 6-8 hrs NPH 12 -20 hrs Ultraiente 18-24 hrs Glargine 24 hrs ```
351
70/30 dosing
most common insulin regimen 70% NPH and 30% regular morning dose covers glucose values before dinner evening covers fasting glusoce
352
explain 70/30 dose adjustment
the patient takes 20 unitls of 70/30 before breakfast and supper but has hypoglycemic symptoms before supper but a consistent fasting Adjust 70/30 to 15 before breakfast and 25 before supper
353
basal bolus isulin
basal one dose bolus based on carbs 1:15 CHO --short acting
354
other DM goals
 Diabetic LDL <125/70 if nephropathy
355
polydipsia, polyuria, polyphagia, fatigue, dyspnea, nausea / vomiting, abdominal pain, dehydration and may have been precipitated by an acute illness, fruity breath, tachycardia, tachypnea met acidosis hyperglycemia
Diabetic ketoacidosis
356
tretment for DKA
IV fluid replacement --noarmal saline at 1000 cc/hr --expect rapid K+ decline with insulin and add 20-30 mEQ KCl/hour if K+ < 5.3 ----hold insulin therapy if admision K+ is < 3.3 Regular insulin NaHCO3 - only if pH < 6.9
357
DKA stymptoms but without met acidosis and diff in treatment
Hyperglycemic Hyperosmolar State Never give bicarb
358
most common cause of hypothyroidism
iodine worldwide | hashimotos in developed countries
359
t4 low | tsh normal
2ry hypothyroidism
360
``` tired dry skin cold poor memory constipagtion weight gain t4 low tsh high ```
hypothryoidism
361
``` floppy baby umbilical hernia large tongue neuro damage pericardial effucsion ```
cretinism
362
hypothyroid tx
t4 replacement levothyroxine at 50mcg wait 3 to 6 weeks to equilibriate
363
``` AI dissorder HLA DR4 may have FH of AI dsease females TSI TSH low t4 high hyperactive heat intolerant palpitations fatigue wt loss thryomegaly tachycardia exopthalmose ```
hyperthyroidism
364
graves treatment
beta blockers (propranolol) sometimes tpo inh --propylthriuracil, methimazole
365
``` average age 60 goiter thyroid lymph infiltrate elevated TSH, low t4, TPO and anti-TG antibodies enlarged cystic nodular thyroid hypothyroid symptoms ```
hashimotos
366
``` Acute onset mimic pharyngits/URI Thyroid tender to palpation hyperthyroid 1 mo - then hypoth 1 mo initially elevated ESR ``` tx
Viral thyroidits Treat with nsaids
367
What compounds and medications interfere with a thyroid uptake and scan
Imaging Studies – Radioactive iodine uptake reflecting thyroid activity; also helpful for thyroid nodules – Beware of iodine-containing contrast media, thyroid medications, etc. for about 6 weeks prior to the scan** – “Hot” (autonomously functioning) nodules are nearly always benign – “Cold” nodules are usually benign, but are more likely malignant than “hot” nodules
368
``` “stones, bones and groans” sually caused by adenoma hypercalcemia hypophospatemia high PTH osteoporosis osteomalcia kidney stones muscle waekness ```
hyperparathyroidism
369
 “classic” subperiosteal bone resorption with prolonged disease, often involvin phalangeal tufts – rarely seen in developed countries anymore
 Osteitis fibrosa cystica | primary hyperparathyroidism
370
gold standard for primary hyperparathyroid
surgical treatment can use calcitrol vit D cinacalcet
371
```  Hypocalcemia  Hyperphosphatemia  Tetany; increased nerve excitability; uncontrolled cramp-like spasms of hand, feet, arms, face Usually Iatrogenic  Convulsions  Trousseau’s Sign positive ``` tx
primary hypoparathyroidism calclium and vit D
372
 Excessive calcium intake along with absorbable alkali (e.g. baking soda) overwhelms kidneys ability to excrete excessive calcium  Hypercalcemia, metabolic alkalosis and renal insufficiency
Milk Alkali syndrome
373
Hypercalcemia Treatment
 Normal saline  Sodium increases calcium excretion; treats (the usually underlying) dehydration  Furosemide  Impairs calcium reabsorption  Bisphosphonates  Impair bone resorption  Calcitonin  Impairs renal calcium reabsorption and bone resorption  Corticosteroids  Increase renal calcium excretion and impair calcium absorption from the gut
374
 Myalgias, muscular weakness, cramps and fasciculations; ultimately tetany  Irritability and paresthesias; ultimately seizures and increased intracranial pressure  Signs  Chvosteck and Trousseau signs May be caused by mg def, vit d def
Hypocalcemia
375
Most common cause – H. Pylori Duodenal (90%) and gastric ulcers (70%) PUD NSAIDs – 2nd tx
ulcers antisecretory therapy plus antibiotics
376
Reflux disease treatment
Antacids (Tums) -intermittent mild symptoms H2 blockers (ranitidine, cimetidine, famotidines) -Mild to moderate, more consistent symptoms -Heals erosive esophagitis in 8 weeks Sucralafate (Carafate) -Bile Reflux Proton Pump inhibitors (Omeprazole, lansoprazole, -prazoles) -All levels of symptoms severity -Heals erosive esophagitis in 4 weeks in 70% of patients -Heals erosive esophagitis in 8 weeks in 90% of patients
377
Difficulty swallowing Most often due to esophagitis, peptic benign stricture Less often cancer of the esophagus or a motility disorder like achalasia usually caused by reflux
dysphagia
378
``` Painful swallowing Most often due to infectious esophagitis Viral like herpes or CMV Fungal like Candida esophagitis Pill induced esophagitis tetracycline, potassium; quinidine and bisphosphonates ```
Odynophagia
379
what do you do first for dyshpagia
If you suspect the dysphagia is due to an esophageal origin should undergo an upper endoscopy If unsure if it is esophageal or pharyngeal do an upper endoscopy to rule out an esophageal cause You don’t want to miss an esophageal malignancy
380
But not in place of endoscopy | Will show Stricture, Mass in esophageal cancer and in peptic stricturs
barium swallow
381
Classic dilated esophagus Bird’s beak appearance Due to tight LES Best seen on Barium Swallow
achalasia
382
History of Reflux or Barrett’s esophagus Now has Solid food dysphagia Weight loss
adenocarcinoma
383
History of Reflux Now has Solid food dysphagia NO weight loss
peptic stricture
384
History of intermittent dysphagia Solids, especially breads and meats No weight loss
Schatzki’s Ring or a Cervical Web
385
scc of esoph
tobacco and alcohol women proximal to mid esop
386
adenocarcinoma of esoph
barretts white males distal esoph/gastric cardia
387
History of intermittent dysphagia Liquids or Solids & Liquids No weight loss
achalasia
388
If patient has rectal Bleed first check
if orthostatic | may need to give fluids or resescetate
389
``` Intermittent Diarrhea without blood Especially young woman May be associated with bloating and abdominal cramps No weight loss Rarely nocturnal diarrhea ```
IBD
390
``` Middle age or eldery Blood mixed with stool Several months Now has lightheadedness Iron Def anemia ``` how to diagnose
Colon cancer colonoscopy
391
``` Elderly History of Coronary Heart disease Few episodes of bloody bowel movement for 1 to 2 days Occurred with abdominal pain Hgb typically drops only 1 or 2 grams ```
Ischemic colitis
392
Any age Very Short duration of bloody diarrhea Associated with ab pain and fever
infectious diarrhea
393
``` Elderly Mult episodes of painless! large bloody bowel movements Primarily made up of blood May be orthostatic Labs show decreased hgb and hct Hgb may drob several grams from baseline If no evidence of upper GI bleed Most common cause of hemodynamically significant lower GI bleed in elderly Aorto-enteric fistula ```
diverticular bleeding
394
Massive bleeding from rectum History of repaired abdominal aortic aneurysm Very unstable due to large amount of bleeding
Aorto-enteric fistula
395
``` Microscopic Found only by positive hemoccult test Clinically significant If Cecal AVM – Red blood or melena If Small Bowel AVM – Melena ```
Bleeding from Arteriovenous Malformations
396
Hematemesis Ab pain History of being on NSAIDs May have coffee grounds as well
PUD
397
History of recurrent non-bloody vomiting followed by bloody vomiting
Mallory Weiss tear
398
Coffee Ground emesis | History of heartbur
esophagitis
399
``` Significant LLQ ab pain Fever No rectal bleeding Middle aged or elderly No diarrhea usually Diagnosed by CT scan NO colonoscopy or barium enema Can cause perforation ```
diverticulitis
400
``` Infection with C difficile Multiple watery bowel movements With or without blood Ab pain and fever Febrile with ab tenderness Nursing patients on oncology floor, following chemo OR any patient following a course of broad-spectrum antibiotics Treat with metronidazole or vancomycin ```
Pseudomembranous colitis
401
Small bowel, especially terminal ileum Transmural inflammation Not usually continuous involvement of the bowel Skip arease – areas of affected bowel interspersed with normal bowel ASCA Cobblestone Colon not usually involved Though it can be Diarrhea but no blood Pain more of a problem for them Diagnosed with colonoscopy Biopsies of terminal ileum, small bowel follow through, and capsule endoscopy Treated with immunosuppressants and immune modulator therapy
Crohns
402
Only affects the colon No small bowel p-ANCA Crypt abscess Superficial ulceration of mucosal lining of colon No skip areas – continuous Rectum always involved Multiple bowel movements every day Small, frequent, soft, water, and can have blood Diagnosed by colonoscopy with biopsies Treated with anti-inflammatory agents and immunosuppression & (at times) immune modulator
Ulcerative colitis
403
Ulcerative colitis and Crohns | Extra-intestinal manifestations
``` Erythema nodosum Pyoderma gangrenosum Arthritis, Iritis Episcleritis ```
404
``` Small bowel disease Presents with diarrhea Large volume No blood Precipitated by ingestion of gluten Protein losing eteropathy due to gluten Actually sensitivity to gluten Diagnosed by blood test for tissue transglutimase antibody AND biopsy of small bowel during an endoscopic exam Biopsy will show flattening of villi AND accumulation of lymphocytes in lamina propria and epithelium Treatment: Avoid food with gluten ```
celiac sprue
405
Used to detect a bleeding site when endoscopy or colonoscopy can’t find OR when patient is bleeding too rapidly to safely do endoscopy Often done prior to angiogram Radio-isotope injected IV into patient Images obtained at different time intervals to determine if a bleeding site can be found To be positive, patient should be bleeding 0.5 cc’s per minute
Tagged RBC scan or Bleeding scan
406
Used to find and treat a bleeding site Catheter into femoral artery Dye injected into superior mesenteric, inferior mesenteric and celiac axis, & vessels they supply If bleeding site found, can use a special coil or glue to embolize the artery (stop the bleeding) To be positive, patient should be bleeding 1.0 cc per minute
angiogram
407
``` History of excessive alcohol use Presents very ill Jaundice and even febrile AST > ALT; neither > 200 Bilirubin > 10, or even 20 High white count, like they have an infection (even though they don’t ```
alcoholic hepatitis
408
History of IV drug use, mult sex partners w/ prostitutes, or dirty needle for tattoo (neighbor) Relatively ill on presentation Viral syndrome – achy all over, febrile Jaundice RUQ tenderness ALT > AST; both in high hundreds or thousands
Hep B acute
409
Presents same as Hep B History of eating in questionable place Or in contact with someone with disease Or workers in Day Care
Hep A
410
Chronic disease Usually asymptomatic, don’t know they have disease History of blood transfusions, IV drugs, tattoo many years ago ALT > AST but only mildly elevated; 100 to 250 Bilirubin normal
Hep C
411
History of attempted suicide or history of injury Took more than recommended dose If alcoholic, less need to have toxic effect ALT > AST; usually very high, like in thousands High bilirubin
Acetaminophen Hepatitis
412
``` History of significant hypotensive event Heart attack or sepsis Asymptomatic relative to liver disease ALT > AST; usually very high, like in thousands Bilirubin normal or slightly elevated ```
Ischemic hepatitis
413
You want to do an elective procedure on a patient with cirrhosis t/f
false
414
hep b vaccinated vs immunity
vaccinated are positive for anti-HBs but not anti-HBc | Immune are positive for both
415
pharm and elderly
elderly have decrease in hepatic and renal metabolism so may need to decrease those drugs
416
bladder innervation
• Parasympathetic (cholinergic) – S2-4: bladder contraction • Sympathetic (alpha adrenergic) – T11-L2: Bladder relaxation; bladder neck and urethral contraction • Somatic – Pudendal nerve: Pelvic floor muscular contraction
417
• Females – Poor anatomic support / urethral dysfunction • e.g., Multiparous female with pelvic floor relaxation (groceries, sneeze, pee) • Males – Sphincter damage • e.g., Urethral sphincter damage from prostate surgery or radiation therapy
stress incontinence
418
• Local GU conditions – e.g., tumor, stone, early obstruction, chr infection, adjacent GI inflamm or diverticulitis • CNS disorders – e.g., stroke, dementia, parkinsonism, SC lesions with impaired sympathetic innervation • Idiopathic – e.g., detrusor instability without GU or CNS disorder Spastic bladder and UTI is usual cause
Urge
419
Dribblers • Anatomic obstruction – e.g., prostate hypertrophy, urethral stricture, large cystocele • Poor bladder contractility – e.g., diabetes, levels spinal cord injury with impaired parasympathetic innervation • Neurogenic – e.g., detrusor-sphincter dyssynergy
Overflow
420
```  Chronic impairments of o Cognitive function o Mobility, Dexterity  Environmental factors  Psychological Factors ```
Functional incontinence
421
Post void residual volume
• BladderScan PVR – Normal is < 200 cc • Very helpful in distinguishing between overflow incontinence and either urge or stress Normal UA but PVR is 300 -> Think overflow like a BPH
422
Treatment for Stress inco
behavior therapis alpha adrenergic estrogen surgery*
423
treatment for urge
behavioral therapies | bladder relaxent drugs
424
treatment for overflow
surgery | catheterization*
425
 Nearsightedness |  Difficulty seeing objects in the distance
myopia
426
 Farsightedness |  Difficulty seeing near objects
hyperopia
427
 Impaired accommodation (ability to focus on close objects)  Greek: “older vision”  Universal; begins at about age 40  Due to gradual age-related lens hardening & dimin muscular effectiveness of the ciliary body  “PERRL” treatment
presbyopia reading glasses or bifocals
428
```  Blurry vision (“dirty glasses”)  Glare / “prism effect”, making it especially difficult to drive at night  Age-related opacities tend to migrate centrally until they interfere with vision  Predisposing factors  Increasing age  Diabetes  Smoking  Alcohol abuse ``` tx
cataracts  Phacoemulsion with intraocular lens implants  YAG laser capsulotomy in about 15% for subsequent capsular opacifications
429
 Most common cause of blindness in the elderly  Characteristically central blindness  Usually excellent peripheral vision
macular degeneration
430
 Drusen (yellow byproducts of metabolism) accumulate under the macula
dry macular degeneration
431
 Increasing drusen accumulation with angiogenesis and choroidal neovascularization
wet macular deg
432
treatment for macular deg
 Ocular vitamins (beta carotene 25,000 units, vit E 400 units, vit C 500 mg and zinc 80 mg)  Laser phototherapy for neovascularization  Intra-vitreal vascular endothelial growth factor inhibitor injections  Stem cell research
433
 Characterized by ischemia, neovascularization, microaneurysms and hemorrhage.  Importance of annual ophthalmologic examinations for diabetics  Glycemic and antihypertensive control are both important
diabetic retinopathy
434
 Optic nerve head damage and visual field loss even with normal intraocular pressures  Usually normal central vision with deteriorating peripheral vision  “Tunnel vision”; “blinders”  Aqueous drainage impairment leads to increased intraocular pressures
glaucoma
435
 aqueous drainage / filtration is slowed  Usually asymptomatic and found on a screening exam by an eye professional  Peripheral visual loss is slow and subtle
open angle glaucoma
436
 Aqueous drainage is blocked  Usually acute and symptomatic  Eye pain; headache; noticeable visual deterioration; possibly nausea and vomiting overshadowing eye pain  Conjunctival injection  May be provoked  Mydriatics; darkness; lens enlargement from growing cataracts; infection; inflammation; trauma, etc
closed angle glaucoma Give emergent treatment acetolzaolmide while in ER
437
Glaucoma Treatment
 Eyedrops to suppress aqueous production (e.g.,beta blockers; alpha agonists)  Beware of systemic beta-blocker effects from eyedrops  Eyedrops to facilitate aqueous outflow (e.g., epinephrine, miotics such as pilocarpine, prostaglandins)  Emergency iridectomy for closed angle glaucoma
438
* Common | * Thinning skin in an older persons external auditory canal produces thicker, drier and more adherent cerumen
Cerumenosis
439
 Generally results from past noise exposure, ototoxic drugs, cochlear neural atrophy or damage (e.g., encephalitis)  Presbycusis (Greek: “older hearing”) • Generally relatively symmetrical and bilateral • High-frequency hearing loss predominates  Phonemic regression • Permanent hearing loss at the CNS level due to lack of stimulation (i.e., the brain “forgets” a frequency, and amplification is no longer helpful) treatment
Sensorineural Hearing Loss programmable digital amplification not hearing aids
440
review rinne / weber
conductive - bone > air (cba) ----localizes to affected ear ssn - air > bone -----localizes to unaffected ear
441
the pathobiology of alzhiemeirs is characterized by
amylid plaques | neurofibrillary tangles
442
summary of dementia/depr/delirium
• Dementia – Progressive cognitive decline; often, the patient “forgets that he forgets” • Depression – “vegetative” symptoms such as lack of motivation (“anhedonia”), sleep disturbances, appetite and weight changes; flat affect • Delirium – Acute onset; delusions and hallucinations
443
A healthy 70-year-old man drank a little more than usual with his friends at the American Legion. He fell, fracturing his hip, which was successfully pinned 3 days ago. His nurse calls you at 10:00 PM because he is agitated, and he claims that the CIA has bugged his hospital room. He most likely has:
delirum
444
An 80-year-old woman complains of memory problems and lightheadedness with exertion during the past year, but she is otherwise healthy, and she takes no medications except for eyedrops for glaucoma. She most likely has:
• C. Beta-blocker-induced dementia
445
• A depressed 80-year-old widow complains that her memory has worsened over the past 6 months. She has also noted generalized muscular weakness, a worsening exercise tolerance, visual disturbances, pedal edema, cold intolerance and easy bruisability during the past 6 months. She most likely has:
hypothroidism
446
A 76 year-old man’s wife complains that his memory has never been the same since his previous doctor gave him “rat poison” for several “spells” of confusion and incoordination. He has an irregularly irregular heart rhythm. The most likely diagnosis is:
• D. Multi-infarct dementia
447
Test Question #2 • A 70 year-old man’s wife complains of his increasingly worsening memory over the past 1 - 2 years. He is becoming more irritable, and he gets lost occasionally when driving his car. He most likely has:
alzheimers
448
A 75 year-old widow who gives a detailed account of her poor memory ever since the death of her husband 6 months ago most likely has:
• C. Pseudodementia / depression
449
spastic hemiparises gait cause
CVA
450
Scissors gait cause
lower extremity spastic paresis from cervical spondylosis
451
assistive devices and uses
``` ASSISTIVE DEVICES • 3- or 4-wheeled walker – e.g., ataxia, hemiparesis, scissors gait • 2-wheeled walker – e.g., Parkinson's • Cane – Antalgic gait • Maladaptive devices – e.g., Don’t use a cane for an ataxic patient ```
452
hyponatreamia def
Na < 133 | determines intravascular volume
453
hyponatremia types and causes
•Hypovolemic hyponatremia: Diuretics, GI losses (e.g. nausea, vomiting, diarrhea, nasogastric suction), severe burn wounds, marathon runner, etc. •Hypervolemic hyponatremia: CHF, nephrotic syndrome, cirrhosis, excessive IV. •Euvolemic (90% of all cases): SIADH, hypothyroidism, Addison's disease • Pseudohyponatremia: Hyperproteinemia, hypertriglyceridemia, hyperglycemia. • Psychogenic: Urine osmolality < 100
454
Hyponatermia treatment
– Acutely altered mental status: 3% saline at 40-50 cc/hr (<12 mEq/24 hr) adjusting rate to increase Na+ by 0.5-0.6 mEq/hr until symptoms improve – Hypervolemic: Fluid restriction, diuretics – Euvolemic: Fluid restriction; treat underlying cause – Psychogenic: Fluid restriction. – Hypovolemic: Normal saline – Pseudohyponatremia: Treat underlying cause
455
Law of consistency: If the pCo2 and HCO3 rise or fall in the same direction and at the rate expected
(HCO3= [1.1 to 1.3] x pCO2
456
how to correct for hypoalbuminemia in met acidosis
– (Expected albumin – observed albumin) x 2.5 + (observed anion gap) is the actual anion gap.
457
metabolic alkalosis causes
»likely diuretics, vomiting, hypokalemia (e.g., aldosteronism)
458
creatinine and GFR relationship
inversely
459
Acute Renal Failure causes
1. Pre Renal 2. Post Renal 3. Renal
460
1. Mucous membranes are dry 2. Tenting of the skin- Where? • Thigh and calf 3. Flat neck veins 4. Orthostatics- Laying/Sitting/standing SBP >20 mm Hg fall,DBP>10 mmHg fall, Pulse increase of >20 5. Wait 3 min between each maneuver Fe Na 20/1 1. Volume loss (GI- N-V-D and diuretics) 2. Relative Vol Loss (CHF,Cirrhosis, Nephrosis, Pancreatitis, Burns, etc) 3. Gastro Intestinal Bleed 4. Hypercatabolic state (Prednisone, Sepsis Neoplasia, Burns) 5. TPN
Pre-Renal Azotemia
461
Post Renal ARFCauses
 Obstruction-Acute, Chronic, Complete, Partial  Hydronephrosis  Usually takes days to develop or to resolve  Ultrasound  Dx- Age related- Reflux,UPJ, Radiation, Prostate cancer, Retroperitoneal Fibrosis
462
```  Fe Na > 3  Bun/Cr < 15/1  U Na >20 1. No Tenting 2. Normal Membranes 3. Hypotension 4. Could be anything ```
Renal ARF
463
Renal causes of ARF
```  Acute Tubular Necrosis 1. Toxins Vs. Ischemia (hypotension) 2. Oligouric Vs. Non-oliguric ARF Oliguria ≡ < 400 cc/24 hours Non-oliguric much better prognostically Glomerulonephritis Glomerulonephritis  Acute- RPGN- Crescent formation  Chronic  Primary Idiopathic  Secondary  Hypocomplementemic  Nephritic  i.e., active urinary sediment with RBCs, etc.  Nephrotic  Overlap ```
464
1. Proteinuria (>3.0 Gms/day)… actually albuminuria 2. Edema 3. Hyperlipidemia ( why?)
Nephrotic syndrome
465
acute interstitial nephritis causes
 Medications- ABX = 71%  Infection = 15%  TINU Syndrome (Tissue interstitial nephritis uveitis syndrome) = 8%  Sarcoidosis = 1%  Drugs = Methacillin/PCNs/Cephalosporins/Cimetidine (rare in other H2 blockers)/ Allopurinol/Rifampin NSAIDS !!!!!!
466
Hyponatremia |  Symptoms- Basically, Altered Mental Status
 Rx- 3% saline at a rate to have serum Na increase by .5 to .6 meq/hr until symptoms improve
467
Again, does not reflect Na stores,rather, total body H20 deficit Sx = Altered mental status  why?- brain cells “shrink”
Hypernatremia
468
hypernatremia treatment
D5W; NOOOOO Salt!!! (e.g., NS, D5 1/2 NS, D5 1/4 NS)
469
 EKG = “U” waves = prolonged QT interval  Muscle weakness  Muscle weakness may be profound; may not be able to walk  Cardiac Arrest K+
hypokalemia treat with K+
470
 K+ 6.0 - 6.5 = Peaked T waves (all leads)  K+ 6.5 - 7.0 = Loss of P waves (EMERGENCY). Increased PR, wide QRS (>120 ms)  K+ of greater than 5.5  Symptoms - same as hypokalemia  Muscle weakness / cardiac arrest / death  Acute hyperkalemia is an urgent problem  Chronic hyperkalemia is not urgent
Hyperkalemia
471
treatment for hyperkalemia
Ca Gluconate immediatley
472
Anion Gap Metabolic Acidosis - MUDPILES
``` Methanol Uremia DKA Paraldehyde Isopropyl alcohol Lactic Acidosis Ethylene Glycol Salicylates ```
473
met acidosis symptoms
 Severe Metabolic acidosis/Resp. Alkalosis  Stimulation of respiratory center tachypnea  Altered mental status = “Salicylate Jag”  Hypokalemia, elevated PT/PTT, hypouricemia, fever  Tinnitus
474
Treatment for met acidosis
```  Alkalinize urine  Cathartic  Replace electrolytes  Dialysis  Bezoar - 35hr peak levels  NEVER SEDATE PATIENT ```
475
Respiratory Acidosis causes
 COPD  End stage ARDS  Iatrogenic  Inability to remove CO2 with ventilation Turn up O2
476
Respiratory Alkalosis
 Hyperventilation |  Causes- Anxiety, Sepsis, Fevers, Gram negative bacteremia, Iatrogenic, Aspirin toxicity
477
Expected changes between co2 and hco3
 Say HCO3- is 14… 24-14 = 10  Expected PCO2 would be: 40 – (a range of 1.1 to 1.3) x 10 = 27 to 29. Expected PCO2 should be between 27 to 29. If higher = Respiratory Acidosis; if lower, Respiratory alkalosis or if C02 is 50, bicarb is 35 to 37
478
4 kinds of kidney stones
calcium - hyperpara, uric acid - hyperuricemia cystine struvite - bacterail enzyme degredation
479
struvite stone tx
remove stone and antibiotic
480
* Generally asymptomatic until stones began to pass into the ureter. * Pain varies from mild to severe (“worse than childbirth”), and generally develops in paroxysms lasting 20-60 minutes. * Upper ureteral or renal pelvic obstruction generally causes flank pain; lower ureteral obstruction causes pain radiating to the ipsilateral testicle or labia, and both pain patterns may be present * Often associated with nausea and vomiting * Occasionally associated with dysuria and urgency when the stone enters the bladder or urethra what imaging do you get
noncontrast helical CT scan ultrasound if preg urinanalysis x-ray if calcium stone
481
medical treatment for kidney stone
``` Encourage fluids for spontaneous passage Pain control – Opioids frequently necessary – NSAIDs fairly effective and may decrease ureteral smooth muscle tone, but might induce ARF and not feasible if vomiting Strain urine for stone analysis ```
482
 May occur spontaneously in younger men  More common after an indwelling Foley catheter  Fever, chills, dysuria / usually very tender prostate*  Usually mild pyuria (8-10 WBCs/HPF)  Positive urine culture more likely following prostate exam treatment
acute prostatitis Usually oxyquinolone or third-generation cephalosporin antibiotics x 10 days
483
 Recurrent acute prostatitis symptoms and/or chronic perineal pain and/or chronic dysuria  Symptoms and rectal tenderness frequently not as pronounced as with acute prostatitis; usually afebrile  Laboratory findings usually unrevealing  PSA not infrequently “artifactually” elevated treatment
chronic prostatitis  Generally requires at least 12 weeks of oxyquinolone antibiotics
484
 Acute pain and often marked swelling of the epididymis  May be associated with prostatitis  Antibiotic treatment as for acute prostatitis  Usually oxyquinoline or third-generation cephalosporin antibiotics x 10 days  Warm baths and NSAIDs usually helpful acutely
Acute Epididymitis
485
• Slow urinary stream • Incomplete emptying • May have urge incontinence early on and then develop overflow incontinence  Usually an enlarged slightly firmer prostate on rectal exam • Possible to have relatively isolated middle / transitional prostate lobe hypertrophy  Post void residual volume is usually increased
BPH
486
BPH treatments
 Alpha adrenergic antagonists (e.g., doxazosin/Cardura; tamsulosin/Flomax) • Reduce prostate smooth muscle tone about the prostatic urethra  5-alpha reductase inhibitors (e.g., finasteride/Proscar) • Inhibit conversion of testosterone to free testosterone, inducing prosthetic atrophy  May result in diminished libido and erectile dysfunction  Usually reduces PSA values by about half; may reduces prostate cancer risk TURP, TUMP, PSV, TVP TIP
487
 Largely obstructive; may be asymptomatic  Signs  Usually a firm nodular mass on rectal exam • Generally, all nodules must be biopsied  PSA usually elevated and/or rising • May be normal (normal values: 0.0-6.2)
Prostate cancer
488
– Hematuria most common, usually painless – Occasional urgency, frequency and dysuria • Diagnosis – Usually by cystoscopic or flexible ureterorenoscopic biopsy – MRI / CT scan
Bladder or renal cancer usually transitional cell cancer
489
• Primarily occurs between ages 20-40 – A testicular mass over age 50 is most likely lymphoma • 2-3 times more likely in an undescended testis – Orchiopexy prior to puberty reverses increased likelihood • Symptoms – Usually a painful testicular mass • A painless testicular mass is very likely cancer if not clearly a varicocele (bag of worms) or hydrocele (transilluminates)
testicular cancer
490
if BRCA-1 or BRCA-2 – “Too late” if discovered on a pelvic exam – Ca-125 tumor marker with transvaginal ultrasonography helpful but debatably reliable
ovarian cancer
491
Usually an abnormal vaginal discharge and abnormal vaginal bleeding, especially postmenopausal bleeding
Endometrial uterine cancer
492
how to diagnose and treat
endometrial biopsy | hysterectomy
493
• Increased risk with multiple sexual partners, likely due to HPV (human papilloma virus) • Diagnosis – Pap smear / colposcopy
cervical cancer
494
most common organism in UTI
e coli
495
– Urgency, freq, dysuria; occasional hematuria and/or an odiferous urine and/or suprapubic pain • Diagnosis – Clinical symptoms; urinalysis and urine culture
Cystitis 3 days of bactrim
496
– Similar to cystitis but may include a vaginal | discharge in females
urethritis caused by chlamydia, gonorrhea and genital herpes
497
– Usually fever, flank pain, nausea and vomiting – Possible present or antecedent symptoms suggesting lower urinary tract infection – May lead to sepsis or renal papillary necrosis • May present as sepsis / septic shock, especially in the elderly and in debilitated and/or demented patients – Often requires hospitalization, IV fluids and IV antibiotics
pyelonephritis
498
gold standard to diagnose uti
urine culture | get a UA too
499
flank pain and intractable vomiting
kidney stone
500
WBC casts ... what is it and what to do
pyelonephritis --- need hospital and IV antibiotics to avoid septic shock
501
Fatty casts
nephrotic syndorme
502
RBC casts
nephritic syndrome
503
ideal BP for a diabetic
125/75
504
where to aim on xray images
``` AP - base of 2nd met lateral - lat cun/cuboid MO - lateral aspect of 3rd met/cun J LO - 1st met cun joint sesamoid - 3rd MPJ calc - achilles insertion ```
505
x-rays rapiopaque and radiolucent
* Radiopaque - Bright | * Radiolucent- Dark
506
filter used in podiatry
2.5mm total
507
how many screens used in podiatry
one
508
controls radiographic contrast.
kvp
509
kvp and subject contrast
high kvp = lower subject contract low kvp = high subject contrast low kvp increases pateint dose
510
determines the number of x-rays produced how much used in podiatry
mA | 15-30
511
exposure time
1/60sec
512
• Patient dose is therefore a function of
mAs
513
• 15% rule
15% change in KVP is equivalent to 2 times of a change in MA | inversely
514
Inverse Square Law
• Radiation intensity is inversely proportional to the square of the distance from the source
515
common source to image distances
40" or 100cm
516
focal spot sized used in podiatry
1MM
517
greatest tool in keeping patient exposure as low as possible
Collimation
518
Summary • Moderate to large SID • Small OID • Collimate to smallest field of view • Heel effect ( cathode side for thicker part) • Grids ( decrease scatter/ increase dose • Screens ( less x-rays needed)
physics
519
words for bright on xray
Synonyms Radiopaque Sclerosis* Eburnation*  opaque -- increase in subject density leads to decrease in optical density. Film appears white.
520
words for dark on xray
Radiolucent Rarefaction* Osteopenia* Osteolysis*  lucent - black areas on film. A decrease subject density leads to increase in optical density.
521
 Bone apposition on xray
 100% is normal  0% is dislocated  Anything between is subluxed
522
m/rems per years for workers
Thus a 20 year old radiology tech is allowed 5 (20-18) which is 10 m/rems per year total body exposure
523
bipartite bones seen
sesamoides med cun navicular (rare)
524
anteater signs
CN coaltion
525
Sclerotic halo usually with flat foot
TC coalition
526
os veselanium
off of 5th met base
527
os peroneum
lateral to cuboid
528
os eccentric interphalanges
prox lateral distal phalanx of hallux
529
os naviculare
deeper in TN joint
530
type II accessory navicular
against navicular but not joint
531
growth plate appearances of foot bones
``` –Base of the phalanges (6 months-3 years) –Heads of the lesser metatarsals (2 years) –Base of 1st metatarsal (1 year) –5th metatarsal base (9-11-years) –Calcaneus (5 years) –Tibia (3 months) –Fibula (6 months) –Posterior talus (8 years) –Sesamoids (10 years) ```
532
primary growth centers are all present at birth except
``` navicular cuboid? lat cun med cun int cun 2ry ossification centers ```
533
apophysis vs epiphysis
• Epiphysis – part of bone that develops separately and then ankyloses. –Common in tubular bones. • Apophysis – outgrowth or swelling of bone. –Tuberosity
534
multiple primary turn into what
bipartites
535
common locations of a pseudoepiphysis
head of 1st met | bases of 2, 3, 4
536
TC coaltion usually seen in 2nd decade and
–Anterior facet – MO –Posterior and middle – calcaneal axial –“C” sign –Talar beaking
537
TN coalition best seen on what view
lateral
538
how does a bone scan work
 Radioisotype (tracer) introduced by IV  WBC may be tagged to specifically address concerns of infection  Tracer is delivered via the vascular system  Tracer attracted to areas of new bone activity/formation  Localization to hydroxyappetite crystals of the bone matrix  Tc --A disruption of bone turnover by a pathologic process on the order of 5 to 15% from normal can be detected by bone scintigraphy - Specificity increases by performing an indium 111-labeled white blood cell test combined with a Technetium-99m-MDP injection.  A“Geiger”gamma camera counter picks up areas of radioactivity  Hot spots = Increased Uptake = Dark Areas  Cold spots = Decreased Uptake = Light Areas  Photograph taken over time (paper chromatography)  Cleared by kidneys and excreted in urine
539
most commonly used bone scan radionuclides | why use
tech 99 good marker of inflammation Good for tumor localization and infection
540
3 phases of a bone scan
Phase I-within 5 min after injection of Tracer – Blood flow phase Phase II-3-5 hrs post injection - Blood Pool/Inflammatory phase Phase III –approximately 24 hrs post injection – Delayed phase 6 hr ½life ½
541
WBC labeled
WBCs migrate to areas of infection localization to bone implies a bone infection Indium-111 labeled WBC, Technetium - 99 labeled WBC (Ceretec) ((HMPAO-Hexamthylpropylamine)  Pts’ leukocytes are separated out and labeled with indium and reinjected into pt  hopefully can be used to assist in differentiation between between OM and Charcot Compare 4 hr tracer to 24 hr tracer, at 24 hrs if tracer still lights up then it is most likely OM
542
bone scan diagnostic value
Any process that induces hyperemic regional blood flow will result in positive in the 1st and 2nd phase Active bony modeling is positive in 3rdphase Infection highly sensitive, but not specific
543
indications for a CT
Imaging of complex structures or pathology Fractures of Midfoot and Rearfoot STJ imaging e.g. tarsal coalitions Evaluation of malunion/nonunions. Preoperative workupof Rearfoot and forefoot reconstruction
544
CT potential problems
Metal may degrade image can give“star burst” Patient has to remain still for up to 30 minutes, may require IV/oral sedation Issues w/possible claustrophobia - unlikely for foot/ankle
545
MRI is good for
 Inflammation, damage to soft tissue especially ligaments and tendons  Soft tissue masses, abscesses and osteomyelitis  Bone lesions (within bone and in cartilage)
546
diff between T1, Spin, T2
```  T1 weighted images  Fat weighted/water suppression  Fat has high intensity signal (white)  Short TR (500ms or less)  Short TE (40ms or less)  Spin Echo  “Stir image”- short time inversion recovery  Water weighted  Long TR (1500ms or greater)  Short TE (40ms or less)  T2 weighted images  Water weighted/fat suppression  Water has high intensity (white)  Long TR (1500ms or greater)  Long TE (90ms or greater) ```
547
MRI Danger
1- Small metal objects may move in the magnetic field and cause damage. Pacemakers and Cochlear implants are typically a contraindication to MRI. 2- Torpedo effect- Magnet can pull any metal object in room into the MRI field( pens, scissors, even wheelchairs 3- TATOOS MAY cause minor discomfort to patient during process.
548
Metal implants
High grade stainless steel, titanium, metal alloys may cause artifacts to show up on image causing blurred image
549
muscle on all mri is always
dark grey
550
MRI with contrast
Contrast increases sensitivity to fluid  E.g. sinus tracts, small abscesses Gadolinium, Iodinated contrast Can be placed IV or into a joint
551
tendon disease on MRI
Tendon DISEASE manifests itself as increased signal intensity- representing edema, myxoid degeneration, inflammation or tear. MRI helps to distinguish acute vs chronic tendonopathy.
552
Magic Angle Effect/ tendon tear Pitfall
Magic angle effect is the phenomenon of anisotropic rotatioin or the 55 degree artifact, giving the false appearance of a tear on T1 On the T2 spin echo dataset, this great signal becomes hypointense and disappears TIPOFF: the normal appearance of surrounding fat and absence of fluid in sheath A true Tear is nearly always accompanied by tendon expansion and inflammatory reaction around the tendon
553
Tendon Tear Classification
 0 Hypointense T1/T2  I. Hyperintense T1, hypointense T2= chronic tear/inflammationor MAE  II. Hyperintense T1&T2= acute a. < 50% tendon area (usually hypertrophic) b. >50% tendon area (hypertrophic or atrophic)  III. Rupture a. Supramalleolar b. Inframalleolar c. Juxtamalleolar
554
- hyperthyroid induced osteopenia: - chronic use of anticonvulsant medication: - deficiency states: - vitamin-D deficiency: (strict vegetarians, no sun or an extremely low fat diet) - gastrointestinal and biliary causes; - renal osteodystrophy - fibrous dysplasia BONE NEVER GETS MINERALIZED FROM GET-GO – SOFT BONES
osteomalacia
555
child Cupping, sclerosis and fraying of metaphysis Pseudofractures-LOOSER’S LINES Poorly mineralized epiphyseal centers with delayed appearance Widening osteoid seams  osteopenia Bowing deformities
rickets
556
EXISTING BONE IS DEMINERALIZED/HYPERMINERALIZED Renal insufficiency and vitamin D deficiency disorders are most relevant Resultant high PTH leaches out the bone Medial side demineralization Sub-periosteal bone resorbtion distal tufts Periosteal lifting Ground glass Lace-like Vascular calcifications
parathyroid disorders osteitis fibrous cystica (browns tumors calcium replaced with fibrous tissue)
557
``` DELAYED FUSION OF EPIPHYSIS DEFORMED OSSIFICATION CENTER/FRAGMENTATION WITH HETEROGENOUS APPEARANCE SHORT SLENDER SHAFTS OF LONG BONES DENSE TRANSVERSE BANDS IN METAPHYSIS WIDE CUPPING OF METAPHYSIS OSTEOPOROSIS OF METAPHYSIS ```
cretinism
558
``` Over 40 male Increasing hat size Bone pain Familial incidence Chronic build-up and break-down of bone A-V shunts CHF Osteosarcoma can result Flame-shaped lesions/”blade of grass” in long bones Osteolytic lesions-OSTEOPOROSIS CIRCUMSCRIPTA Sclerotic bone mixed with lytic bone Bowed limbs, fail; Fractures, including "banana" or "chalk" transverse fractures “picture frame” vertebral body ```
Pagets disease (osteitis deformans)
559
BONE RESORBTION – OSTEOPOROSIS EXOSTOSES ON LATERAL BORDER OF THE METAPHYSIS-Pelkan Spur “GROUND GLASS” INCREASED DENSITY AT METAPHYSIS-Frankel line SCURVY LINE: lucent line on shaft side of Frankel line CALCIFICATION OF SUBPERIOSTEAL HEMORRHAGE WINBERG’S SIGN - sclerotic line surrounding epiphysis
scurvy
560
``` DECREASED DENSITY IN LONG BONES TRABECLAR COARSENING CORTICAL THICKENING DESTRUCTIVE LESIONS-INFARCTS MOTTLING-moth eaten Long slender bones SALMONELLA OSTEOMYELITIS PERIOSTEAL NEW BONE-BONE WITHIN A BONE BRACHYMETATARSIA from infarcts at growth centers DACTYLITIS with edema ```
sickle cell
561
ELONGATION & THINNING OF LONG BONES ARACHNODACTLY ABNORMAL COLLAGEN
marfans
562
* EXOSTOSIS * Joint Mice * Lipping * “Dorsal Flag” * Eburnation * Sub-Chondral * Sclerosis * Joint Space Narrowing * Joint Surface * Flattening * Ankylosis * Arthrodesis * Heberden’s Nodes * Bouchard’s Nodes
OA
563
* Juxta-articular Cysts * Juxta-articular * Erosions * Joint Subluxation * Joint Dislocation * Osteoporosis * Osteopenia * osteomyelitis * Demineralization
RA
564
* Effusion--Early * Joint Space Narrowing--Late * “Punched Out Lesions” * Overhanging Margins * Martel’s Sign
Gout
565
* “Fluffy Heel Spur” * Ankylosing Spondylitis * Sacroiliitis * Vertebral Squaring * SHINING CORNERS * Syndesmophytes * Bony Bridging * Bamboo Spine * “Fluffy Heel Spur”
Reactive Reiter's
566
* Erosions * Sacroiliitis * Terminal Whittling of Proximal Bone * “Pencil in Cup” * ARTHRITIS MUTILANS * Sausage Toe
Psoriatic arthritis
567
Factors to be considered on all chest x-rays include
``` Inspiration Penetration Rotation Angulation Orientation ```
568
Fluffy upper lobe infiltrates | Could be cocci, but can’t make that diagnose on xray
TB
569
airspace disease associated with consolidation (coming together to form a mass). There is no volume loss. The air spaces are filled with a water density from the inflammation associated with microorganisms and pus. Most common infectious cause of death in U.S
Pneumonia
570
Thin walled cavity think what | Thick
thin - TB, Cocci, WB | Thick -> lung/mass tumor
571
enlarged heart on cxr, what test do you get next
Echo | could be pericardial effusion or cardiomegaly
572
pneumothorax treatment
Treatment is to put on O2 or a breathing tube | Recognize if mediastinum is shifted (Tension
573
SOB, previous DVT | get what test
CT angiography | VQ scan is second but a poor choice
574
COPD signs on chest x-ray
enlargement of retrosternal space and diaphragm flattening
575
CT considerations
Check all menstruating Female pt pregnancy status. Please note many teens will not be truthful about sexual activity. CTs irradiate the pt! •Think twice before ordering. •Only order when necessary. •Don’t do imaging without a purpose. •Know what you’re going to do with the information. •Will the results change your management?
576
Contra-Indications to IV Contrast
Iodine Allergy | Renal Failure & Not on Dialysis (Based on BUN/Cr and GFR)
577
Foreign Bodies imaging choice
ultrasound
578
Salter Harris Classifications
``` 1 – transverse thru GP 2 – GP and Meta 3 – GP and Epiphysis 4 – GP and Meta and Epiphysis 5 – Crush injury ```
579
Fracture from FOOSH from normal height
Refer to orthopedic surgeon | Dexa scan if fragility fracture
580
MRI considerations
No metal allowed Dress in hospital gown No bras or hair clips Orthopedic implants ok (except eye for brain) Welders -> get plain film of orbit! Most pacemakers and defribillators not allowed Beware of shrapnel Closed Scanner -> better image quality, but can cause claustrophobia Open -> more comfortable but poorer image 30 to 60 mins Loud noise 400 to 3000 dollars
581
Acute Appendicitis imaging
US in kids | CT in adults
582
Gallstones imaging
ultrasound
583
DVT Dopper things to look for
Compression Color Flow Augmentation
584
metastasis to bone | sclerotic and lytic
Sclerotic: Prostate, Lung, Breast Lytic: Breast, Lung, Renal Cell, Thyroid, MM
585
Complications of pagets
``` Pathological fractures 2ry Osteoarthritis Bony deformities Deafness Spinal Stenosis High output CHF Osteosarcomas ```
586
how to differ bakers from dvt
Ultrasound | MR if ruptured
587
atlanto-axial subluxation seen in what
rheumatoid
588
avn commonm places
1. Femoral Head 2. Humerus 3. Knee 4. Talus
589
``` SI involvement bilateral syndesmophytes enthsitis whiskering bamboo spine \ ```
ankylosing spondylitis
590
``` asymmetry DIP early widening of joint later narrowing pencil in cup ```
psoriatic arthritis
591
grading edema
* 0- no edema present * 1- mild * 2- moderate * 3-moderate to severe * 4-severe
592
• Valleix Phenomenon
– Percussion of the nerve causing proximal and distal radiation or paresthesias
593
muscle strenght testing
0 No muscle contraction is detected 1 A trace contraction is noted in the muscle by palpating the muscle while the patient attempts to contract it. 2 The patient is able to actively move the muscle when gravity is eliminated. 3 The pt may move the muscle against gravity but not against resistance from the examiner. 4 The patient may move the muscle group against some resistance from the examiner. 5 The patient moves the muscle group and overcomes the resistance of the examiner. This is normal muscle strength
594
inflammation of vein with blood clot (thrombus) formation (superficial & deep
thrombophlebitis
595
painless, insidious swelling of the Tissues leadiang to decreased function of the lymphatic system. May be congenital or acquired
lymphedema
596
Arthritic classes by synovial class
``` I - non-inflmmatory (OA, ON, Charcot) II - inflammatory (RA, etc) III - septic IV - hemorrhagic ---trauma, PigVillSyn, TB, Neoplasia, Charcot, coagulopathy ```
597
Class I synovial fluid findings
``` Clear/yellow Transparent WBC < 2,000 <25% pMNs Culture negative ```
598
ClassII Synovial findings
``` Yellow/White Translucent/opaque WBC 2,k to 100k > 50%pMNs culture neg ```
599
Class III synovial findings
``` yellow/white Opaque > 100k WBC > 95% PMNs Culture positive ```
600
Class IV synovial findings
Red | Opaque
601
physical findings of OA
firm swelling around joint crepitus restricted ROM
602
OA common joints
``` hips knees 1st carpal metacarpal joint 1st MTP PIP, DIP ```
603
RA common joints
wrists MCP ankles MTP
604
lab tests for RA
``` high ESR high CRP' post rf pos ccp anemia ```
605
ACR criteria for RA
``` Morning stiffness > 1 hour 4 or more Arthritis of >3 joint areas Arthritis of hand joints (MCPs, PIPs, wrists) Symmetric swelling (arthritis) Serum rheumatoid factor Rheumatoid nodules Radiographic changes ```
606
extra-articular features of RA
``` Anemia (most common extra-articular feature) Nodules – elbows, achilles Lung disease: fibrosis, nodules, pleural Cardiac: pericarditis Vasculitis FeltySyndrome Sjogrens syndrome Lymphadenopathy ```
607
treatment for RA
- NSAIDS (pros and cons) - Corticosteroids (lowest dose possible) - Methotrexate – start at 7.5 or 10mg/week, monitor CBC, Renal, LFT, albumin - DMARDS
608
``` Foreign body sensation (sandy or gritty) Dry or decreased tearing Burning Photosensitivity Itching Filmy sensation ```
sjogrens syndrome
609
``` RA Splenomegaly Neutropenia Other Features Anemia Thrombocytopenia Lymphadenopathy Leg Ulcers Skin Pigmentation ```
Felty Syndrome
610
5 clinical syndromes of Psoriatic arthritis
``` Asymmetric oligoarticular Symmetric polyarticular Arthritis Mutilans DIP Only Axial Skeleton ```
611
definitive diagnosis of gout
“the definitive diagnosis is possible only by aspirating and inspecting synovial fluid or tophaceous material and demonstrating needle shaped monodsoium urate crystals with negative birefringence under polarized microscopy
612
treatment for asymptomatic hyperuricemia
nothing
613
uricosurics
probenicid
614
xanthine oxidase inh
allopurinol (start at 100) Feuxostat - hepatic glucoronidation 40mg start
615
``` PMales over 60 Knee chondrocalcinosis often degenerative Crystalls CPPD Small rod like positive birefringence ```
pseudogout
616
``` Inflammatory back pain: Lumbar or buttock pain lasting> 3mo. pg Alternating buttock pain Pain worse c rest Pain improves c activity Back stiffness> 30 min Pain awakening pt. in the second half of the night* Consider what ```
spondyloarthropathy
617
Seronegative Diseases Share
``` 1. Enthesitis 2 Axial arthritis 3. Peripheral arthritis 4. Tendency toward new bone formation 5. Extraarticular features 6. THE HLA B27 ANTIGEN ```
618
Prototype of the seronegative spondyloarthropathies Clear link c HLA Clear link c HLA--B27 mechanism ??? Usually presents c backpain Male predominance but women do get it (3:1) Enthesitis -- enthesopathy Peripheral arthritis New bone formers  Extraspinal manifestations: Eye-acute anterioruveitis Heart-- aortic insufficiency Lung--apical disease
ankylosing spondylitis
619
Seronegative asymmetric arthropathy (predominantly lower extremity) Plusone or more of the following –– Urethritis/cervicitis –– Dysentery Dysentery –Inflammatory eye disease –– Mucocutaneous disease: balanitis, oral ulceration, keratodermia
reactive arthritis
620
diabetic complications
heart disease blindness kidney disease amputation
621
Tissue changes in diabetes
 Altered protein function and turnover, cytokine activation  Osmotic and oxidative stress  Reduced motor and sensory nerve conduction velocity  Increased glomerular filtration rate and renal plasma flow
622
pedal complications in diabetes
``` Neuropathy Vasculopathy Immunopathy Limited Joint Motion Ulcerationi Infection Gangrene Charcot Collapse ```
623
unholy triad
Neuropathy….….loss of sensation to extremities Vasculopathy …..decreased blood flow Immunopathy…..inability to fight infection
624
risk stratification for diabetics
0 - normal - q12 m 1 - PN - q6 m 2 - LOPS, deformity, PAD, q3m 3 - Previous ulcer or amp q1-3m
625
wagner wound classification
 Grade 0: No open lesions  Grade 1: Superficial Ulcer  Grade 2: Deep Ulcer  Involves ligament, tendon, joint capsule or fascia  No abscess or osteomyelitis  Grade 3: Deep ulcer with abscess, osteomyelitis, or joint sepsis  Grade 4: Local Gangrene of forefoot or heel  Grade 5: Extensive gangrene of entire foot
626
UNIVERSITY OF TEXAS WOUND CLASSIFICATION
Stages  Stage A: No infection or ischemia  Stage B: Infection present  Stage C: Ischemia present  Stage D: Infection and ischemia present Grading  Grade 0: Epithelialized wound/no wound  Grade 1: Superficial wound  Grade 2: Wound penetrates to tendon or capsule  Grade 3: Wound penetrates to bone or joint
627
* ‘Pain arising as a direct consequence of abnormalities in the somatosensory system in people with diabetes.’ * A diagnosis of exclusion and is a clinical diagnosis
diabetic neuropathy
628
PN large fiber vs small fiber
``` Large fiber ▫ Large myelinated fibers (5% of nerves) ▫ Touch, vibratory sense, proprioception ▫ Late finding ▫ Severe disease ▫ Stabbing or shooting symptoms are most common of nerves) ``` ``` Small Fiber ▫ Unmyelinated and small myelinated nerves (95% f ) ▫ Pain, temperature ▫ Earliest finding ▫ Documentable changes precede symptoms ▫ Burning is most common ```
629
diabetic PN motor neuropathy
``` Proximal Amyotrophy-presents with pain, atrophy, and weakness (difficulty standing up, climbing stairs) Unilateral Weight loss Distal Intrinsic muscle wasting Hammertoes Hallux limitus Equinus ```
630
= Rapidly reversible sensory symptoms in poorly controlled diabetic patients during episodes of elevated blood sugar.
hyperglycemic neuropathy
631
= Asymptomatic neuropathy becomes temporarily symptomatic with rapid drop in blood sugar
“Insulin Neuritis”
632
PN best prevention tool
normoglycemia
633
therapeutic options for PN
``` •Symptom Relieving Only ▫ Physical modalities ▫ Antidepressants ▫ Anticonvulsants •Disease Modifying ▫ Intensive glucose management ▫ Antioxidants/nutriceuticals ▫ Decompression ```
634
meds used for PN
TCA (amitriptyline) SNRI (cymbalta, effecxor) anticonvulsants (gabapentin, Lyrica) Opiods (tramadol) Membrane stabilizers (Lidocaine, Mexilitine) Nutriceutilcals (b-complex, alpha lipoid acid, folate, vit C)
635
Major predisposing factor for DFI is
DF ulcer
636
evidence of infection in DFU
Redness, warmth, swelling, tenderness, or pain | Purulent secretions, undermining of skin edges, foul odor
637
Factors that increase risk of infection:
Probe-to-bone test +, >30 days, recurrent ulcer, PVD | LOPS, renal insufficiency, barefoot walker
638
Clinical Classification of a Diabetic Foot Infection
Uninfected or Grade 1: No signs of infection. Mild or Grade 2: Locally infected ulcer Moderate or Grade 3: Foot or limb threatening. Severe or Grade 4: Life threatening.
639
• Granulation tissue base • No deep tracts • No cellulitis o Most diabetics will respond with cellulitis • No purulence o Serous drainage = normal • Wound lacking purulence or anymanifestation of inflammation.
Grade 1
640
* Presence of ≥2 manifestations of inflammation. * Cellulitis that extends ≤2cm around the ulcer. * Infection is limited to skin or superficial subcutaneous tissues. * No other local complications or systemic illness.
Grade 2
641
• Infection in patient who is systemically well and metabolically stable. o Has ≥ 1 of the following characteristics: o Cellulitis extending ≥2cm, o Lymphangitic streaking, o Spread beneath the superficial fascia, o Deep tissue abscess, o Gangrene, o Involves the muscle, tendon, joint and/or bone.
Grade 3
642
Signs of a Limb-Threatening Infection
``` Evidence of systemic inflammatory response Rapid progression of infection Extensive necrosis or gangrene Crepitus on examination Soft tissue gas on imaging Bullae, especially hemorrhagic New onset wound anesthesia Pain out of proportion to clinical findings Recent loss of neurologic function Critical Limb Ischemia Extensive soft tissue loss Extensive bony destruction Failure of infection to improve with appropriate therapy ```
643
Infection in patient with systemic toxicity or metabolicinstability. Examples include; fever, chills, tachycardia, hypotension, confusion, vomiting, leukocytosis, acidosis, severe hyperglycemia, or azotemia.
Clinical Classification of a DFI Grade 4: Severe
644
avoid prescribing antibiotic for what
uninfected ulcers
645
when treating DFU as outpatient
``` Stabilize the patient In office I&D Deep tissue culture Appropriate antibiotic coverage –this may be adjusted on follow up or with culture results Appropriate shoe wear/off-loading Appropriate wound care ```
646
Treatment of Infection -When treating in hospital;
Stabilize patient Obtain appropriate labs, studies and consults. Surgical I&D, deep cultures, post-op management and appropriate antibiotics. Discharge as soon as patient able.
647
if patient had MRSA in past.....
treat them for MRSA
648
common topicals and how long to use
``` IDSA recommend use for 1-2 weeks only. Common examples: Mupirocin Silver compounds (incl: Silvadene) Iodine compounds (incl: Betadine) Gentamicin/Triple Abx preparations Transition to wound gel once infection controlled ```
649
IDSA indication for soft tissue infections with oral meds
2-4 weeks of oral antibiotics. | For osteomyelitis: up to 3 months combined therapy.
650
indications for IV antibiotics
Typically reserved for Limb or Life Threatening DFI’s. Generally started in a hospital setting. The selection of the antibiotic is often hospital directed. If MRSA suspected, or patient history, the patient will be empirically covered. Infectious disease (ID) consults helpful in determining appropriate coverage.
651
mild Staph aurues infection
Keflex Augmentin (amox/clav) Clinda
652
mild MRSA infection
Doxycycline | Bactrim
653
moderate staph infection
ampicillin-sulbactam ertapenem imipenem
654
moderate to severe MRSA
Vancomycin Linezolid Daptomycin
655
Pseudomona infection
mild - quinolones | mod - Pipercillin tazobactam (zosyn) (broad)
656
definitive diagnosis of osteomyelitis
bone biopsy
657
plain radiographs for osteomyelitis
``` Periosteal reaction/elevation Loss of cortex with bony erosion Loss of trabecular pattern or marrow radiolucency New bone formation Bone sclerosis with or without erosion ```
658
```  Classic periwound signs  Brawny edema  Hyperpigmentation  Lipodermatosclerosis  Located in the gaiter (supramalleolar) region  Irregular borders  Copious drainage  Beefy red base  Painful ```
venous ulcers
659
```  Classic peri-wound signs and symptoms  Weak pulses/delayed capillary refill  Skin shiny, atrophic, dry  Intermittent claudication or rest pain  Location typically dorsal, distal and over bony prominences  No drainage  Pale base  Black eschar often found  Very painful ```
Arterial (Ischemic) Ulcers
660
``` Classic associated findings Diminished sensation Poorly controlled DM Located plantarly Round with peri-wound callus and undermining Painless Base is variable Drainage is variable ```
diabetic ulcers
661
``` Classic historical findings Institutionalized patient Immobile or confined to bed May have DM, VI, or PAD Always located over bony prominences Often painful but not always Base may be pale/black if ischemic Often very deep ```
Pressure ulcers
662
Most common cutaneousmarker of diabetes (present in 40 -50% of diabetic patients) Sign of increased likelihood of internal complications Males > females (2:1) Shins & feet Round, flat red papules Fine Scale Depressed hyperpigmented areas may appear later Caused by microangiopathy May be confused with psoriasis (different histopathology) and with NLD (not waxy or shiny) Rarely symptomatic but may respond to corticosteroid cream (use care in the pretibial region) Keep skin moisturized Control blood sugar
diabetic dermopathy
663
``` Abrupt appearance Acral location (Acral = away from central trunk) Porphyrin levels Immunoflourescence Intraepidermal Subepidermal no hx of trauma ```
bullosis diabeticorum
664
``` Clear, non hemorrhagic Non-inflammed base Tips of toes and fingers Long--standing diabetes Peripheral neuropathy Good circulation Heals without scarring NO HISTORY OF TRAUMA ```
intraepidermal blisters of BullDiab
665
``` May be hemorrhagic Non-inflammed base Tips of toes & fingers, NWB Areas Heals with scarringand atrophy NO HISTORYOF TRAUMA ```
subepidermal blisters of bulldiab
666
``` Collagen degeneration w/ granulomatous response Initial lesion often red or violaceous papule/patch Lesions enlarge into -–Sharply demarcated ––Indurated, waxy appearing –– Depressed or atrophic –– Yellow-brown plaques –– Raised borders –– Telangiectasia common Most common on shins Most commonly bilateral May precede precede the diagnosis of diabetes in 15% Lesional anesthesia is a hallmark ```
Necrobiosis Lipoidica (Diabeticorum)
667
considerations for Necrobiosis Lipoidica
``` malignant transformation (biopsy it) biopsy ```
668
treatment of NLD
topical steroids | intralesional steroids