Boards Part 2 Flashcards
Pacemaker for
• 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)
Most common cause of tachycardia
re-entry
types of supraventricular tachycardia
- Sinus tachycardia
- Paroxysmal supraventricular tachycardia (PSVT)
- Sick sinus syndrome (SSS)
- Wolff-Parkinson-White/Lown-Ganong-Levine (WWW/LGL)
- Atrial flutter
- Atrial fibrillation
sinus tachycardia cause and tx
irritable SA node or atrial focus
Treat primary disorder (rehydrate, o2)
PSVT tx
Vagal manuevers (80%) IV Adenosine or overdrive pacing
BB, CCB, Dig are preventitive
Short PR interval (<.12 sec)
Congenital accessory AV pathway
Tx for it
Wolff-Parkinson Whjite
Radiofrequency ablation is TOC
Sawtooth pattern seen in mitral stenosis, pericarditis and ARF
Atrial flutter
Irregularly irregluar rhythm
tx
Atrial fib
Rate control with BB or CCB
CVA proph with warfarin if chronic
> 3 cons PVCs
Vent Tachycardia
can be paired, multifocal or frequent
can lead to v fib
v tach etiology
- Usually due to ischemic heart disease and/or an acute myocardial infarction
- Prolonged QT syndrome
- Familial
* 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
Stable Angina
- Relieved with rest, O2, nitroglycerin
medical tx for CAD
- 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
interventional tx for CAD
- PTCA/stent
- Atherectomy
- CABG
- Progressively diminished exercise tolerance
- Increasing frequency and severity
- Relatively recent onset
(unstable angina with elevated biomarkers)
tx
Unstable Crescendo
Non-ST elevation MI
Immediate Hospitalization
O2, nitrates, BB, Anti-thrombotic tx
- Usually abrupt, severe and persistent
- EKG
- Biomarkers (CPK-MB; troponin-I; SGOT; LDH)
Tx
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
- 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
Prinzmetal’s Angina
- Nitroglycerin
- Calcium channel blockers
- Asymptomatic MI
- May present with post MI complications (e.g., CHF)
- Frequent in diabetics
- “Autonomic dysfunction” prevents chest pain sensation during M
Silent MI
- 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
GERD
Causes of Chest Wall Pain
- Usually some form of trauma/strain
– ? Severe coughing paroxysm
– ? Heavy lifting, etc. - Often pleuritic
- 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)
Pericarditis
- Severe, abrupt, radiating to the back
- Physical exam:
– ? Loss of lower extremity pulses
– Possible murmur of AI
Chest Pain Secondary to Aortic Dissection
Chest Pain
- Variable and usually atypical pattern
- Often associated with a history of anxiety and depression
- Often precipitated by situational factors
- Diagnosis by exclusion
Psychophysiological Chest Pain
HTN goals for blacks w/ and w/out organ damage
135/85 if none
130/80 is evidence
HTN definitions
- Normal BP 120.
* Isolated systolic hypertension: Systolic BP >139, normal diastolic BP
aldoseterone does what
Causes Renal Na retention to increase blood volume
Hypertension with not direct cause
Risk factors – Genetics – Sodium consumption – Obesity – Alcohol abuse – Type 2 diabetes – Type “A” personality
Essential HTN
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
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
HTN with hypokalemia tx
Spironolactone
– 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
– 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
– 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
– 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
– 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
HR that compromise perfusion
Generally HR 140 compromises perfusion due to inadequate time for sufficient preload
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
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
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
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
Lab for CHF
Blood work: CBC, CMP, TSH, UA, NT pro-BNP (byproduct of stretching myocytes)
tx for CHF
Diuretics Sodium restriction BB ACEi Digoxin Vasodilators
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
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
Pulmonary Hypertension Treatment
Treat underlying cause
Oxygen
Vasodilators
– Calcium channel blockers; ? sildenafil (Viagra)
Classifications of cardiomyopathies
- Dilated
- Hypertrophic
- Restrictive
- 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
- 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
- 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)
- 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
- 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
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
Opening snap rumpble augmented with exercise right CHF findings EKG: LAE Can have A fib
Mitral stenosis
• 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
– 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
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
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
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
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
Acquired dyslipidemia
obesity Type 2 DM Hypothyroidism Liver Disease Renal Disease
Treatment goals for risk factors
0 – 2 <70
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
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
combo therapy for elevated cholesterol beware of what combo and why
Beware of statin/fibrate combination (myositis; rhabdomyolysis; elevated CPK)
meds for cholesterol and what they target
LDL only - Statin
LDL, HDL, TG - Niacin
TG only - Fibric acid derivatives
LDL - Ezetimibe
Big QRS
Compensatory pause
PVC
PVC falls on what wave cause vent tachycardia
T wave
torsade de pointes (Vent fib with twisting axis) cause
Congential QT syndrome
Long PR consistently prolonged
1 deg AV block
PR interval consistently increases in successive cycles
lack of QRS
Wenkenbach 2 AV block
2:1 P to QRS
Mobitz 2 AV block
3:1 P to QRS
Mobitz 3 AV block
PR interval not the same
Normal QRS
3 AV block
bunny ears
Bundle branch block
Diphasic P wave
RAH or LAH
Large R wave in V1
RVH
Large S wave in V1
Large R wave in V5
LVH
t wave inversion
ischemia
ST elevation
Injury
ST depression
subendocardial infarction
positive stress test
digitalis
significant q waves
infarctions
infarct leads
sig q waves
I and AVL = Lateral
V1, V2, V3, V4 = Anterior
II, III, AVF = inferior
U waves
hypokalemia
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
Arterial Blood Gas Analysis PaO2: Measure of Oxygenation
Arterial Blood Gas Analysis PaCO2: Measure of
Ventilation
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
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
PFTs in Obstructive Lung Disease
• Spirometry
- Low FEV1/FVC (12%) in asthma
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
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
Assessment of bronchospasm of Asthma
• Spirometry: FEV1 • Peak flow meter • Use of bronchodilators • Symptoms - Particularly nighttime awakenings
FEV1/FVC improves with dilator
Asthma
Signs of poor control of asthma
(rule of 2s)
- Use “rescue” meds >2 times/week
- Nighttime awakening due to breathing >2 times/month
• Defines a severe asthmatic episode that is not responsive to repeated treatments with usual
inhaled medications
Status Asthmaticus
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)
best way to improve COPD
smoking cessation
Low flattented diaphragm
increased AP diameter
Air trapping
COPD
Therapy in COPD
• Smoking Cessation • Drug Therapy --B2 agonists, anticholinergics • Oxygen Therapy • Exercise/Nutrition • Lung Volume Reduction • Lung Transplantation
• 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
Restrictive lung diseases
- Interstitial Lung Disease
- Neuromuscular Disease
- Severe Obesity
- Chest Wall/Spine Deformity
- Pleural Disease
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
• 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
- Military Exposure (ships/tanks)
- Ship-Building
- Boiler worker
- Electrician
- Brake Repair
- Construction
- Building Remodeling
ILD: Asbestos
- Mining
- Sand-blasting
- Metal working
- Glass workers
ILD:Silica
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
Hypersensitivity Pneumonitis ILD
exposure to organic dusts
agriculture, moldy hay
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
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
Sarcoid Dx
• Radiographic - Hilar/Mediastinal Adenopathy - Pulmonary Infiltrates • Pathologic - Granulomas: Non-caseating
• 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
Treatment of ILD
• Known Causes - Avoid/eliminate exposure - Corticosteroids • Sarcoidosis - Corticosteroids - Methotrexate • Idiopathic Pulmonary Fibrosis - No proven therapy, ? Pirfenidone - Transplant
ARF types
• Hypoxemic Respiratory Failure
- Low Oxygen Level
• Hypercapnic Respiratory Failure
- High Carbon Dioxide Level
• 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
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)
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
Cause of death in Hypoxemic Resp failure
infectious complications
- 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
some causes of hypercapnic resp failure
• Advanced COPD - Severe COPD Exacerbation • Severe Asthma - Status Asthmaticus • Neuromuscular Disease • Hypoventilation - Trauma, stroke, drug effect, over-sedation
most common presenting symptom of lung cancer
cough
syptoms of lung cancer
- cough
- Hemoptysis
- Wheeze, shortness of breath
- Dysphagia
- Weight loss
- Chest discomfort
- Signs of metastatic disease
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
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)
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
Methods to stage lung cancer
CT scan
PET scan
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.
what if you see a neoplasm in the airways
neoplasm (not cocci)
early diagnosis of lung cancer
Routine CT scans
lung cancer metastases sites
bone
brain
liver
adrenal glands
cancer of surface of lung (pleura) often related to asbestos exposure
Mesothelioma
metastatic disease to lungs
Breast
Colon
Kidney
Melanoma
common cold causes and tx
rhinovirus
no antibiotics
treat with tylenol, etcc
• 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
• Usually viral
• 15% Strep
- Exudate with fever and lymphadenopathy
tx
Acute pharyngitis
Penicillin or erythromycin
- Usually posterior cervical adenopathy, a dull white exudate and possible hepatomegaly or
splenomegaly - Rash if given amoxicillin
Mononucelosis
Penicillin or erythromycin
Acute sinusitis
Narrow spectrum antibiotics
Amoxicillin or Bactrim
sinus obstruction > 12 weeks cause
bacterial or fungal
get sinus CT
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)
usually bacterial following a viral URI
- S. pneumoniae; H. influenza; M. catarrhalis
- RX: amoxicillin although 1/3 resistant; treatment debatable
otitis media
tx for serous otitis media
- Consider antibiotics and/or myringotomy tubes if significant hearing loss and effusion > 3 mo
- Potentially fatal
- Dx: Lateral neck films ; cherry red epiglottis with fiberoptic rhino-laryngoscopy
acute epiglottiis
ampicillin/sulbactam or 2/3 cephalosporin
maybe hospitalization
usually viral
• Characterized by cough, usually with sputum production
• The absence of abnormalities on chest radiography distinguishes from pneumonia
acute bronchitis
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)
• Primary symptom is chest pain, worse with inspiration
• Usually viral
• Treat symptomatically
- Non-steroidal anti-inflammatory drugs
Pleurisy
URI and LRI
What are LRIs
pneumonias
• 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
symptoms of pnuemonia
- Cough, usually productive
- Fever, chills
- Dyspnea
- Malaise
- ? Confusion
- Symptoms may vary from severe to absent
Physical Findings in Pneumonia
• Fever and tachycardia
• Tachypnea (RR > 20)
• Auscultation of chest
- Common: Crackles (“rales”)
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
Clinical Signs of Severe Pneumonia
• Hypoxemia - SaO2 < 92% • Tachycardia • Hypotension • Altered mental status - Obtundation - Confusion
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
walkling pneumonia
- Some organisms (mycoplasma or chlamydia) may cause mild symptoms
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
• 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
- Evidence of tuberculosis organisms multiplying in pulmonary or extra-pulmonary site
- Often infectious to others
active TB
- Cough and minor symptoms for 2-4 weeks and central infiltrates on chest x-ray
- Usually not infectious
Primary TB
- “reactivated” tuberculosis; symptoms may be similar to pneumonia with peripheral and apical
chest x-ray infiltrates - Infectious
2ry TB
- Cough
- Weight loss
- Fatigue
- Fever and night sweats
- Sputum production
- Hemoptysis (usually late in disease)
- Dyspnea
TB symptoms
reactivation TB usually involves what
upper lobes
cavity will form
• Patients with a positive Tb skin test, but no evidence of active tuberculosis have what is
termed
latent tb
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
TB test interpretation
• Positive
- ≥ 10 mm induration
- ≥ 5 mm if:
- HIV
- Immunosuppressed
- Recent close contact
- Radiographic evidence of old TB
Latent TB tx
isoniazid 9 months with B-6
Active TB tx
isoniazid plus B6
Ethambutol
Rifampin
Pyrazinamide
DVT study
Duplex ultrasound
- Pleuritic pain or hemoptysis 65%
- Isolated dyspnea 22%
- Circulatory collapse 8%
No dyspnea is present 27%
Tachypnea (>20) 70%
Tachycardia (>100) 43%
Crackles (rales) 53%
PE
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
Diagnosis of PE
Spiral CT! (contrast enhanced)
VQ scan
D-dimer (sensitive to rule out)
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
MICROCYTIC ANEMIAS
- IDA
- ACD
- Hemoglobinopathy (eg THAL)
- Sideroblastic anemias (lead poisoning)
• 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
• Characterized by: – ↓Fe – ↑↑Ferritin – ↓ EPO • Develops in: – Chronic infections – Chronic inflammatory disease – Neoplastic disease
anemia of chronic disease
Macrocytic = megalo & non-megalo
Name causes of megaloblastic (oval) anemias
• B12/Folate def • Drugs: – dilantin/OC – hydrea/methotrexate • Some marrow disorders
– ↑ RBC Mass – Normal O2 – Splenomegaly – Increased: WBC / PLTS / B12 / LAP score – JAK-2 Mutation – Bone Marrow Hypercellularity
Primary Polycythemia vera
polycthemia vera tx
– Phlebotomy (do it until hct under 45)
• H/H < 15/45 – decreases thrombotic risk
– Hydroxyurea
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
– Rapid pallor / anemia – Jaundice – Splenomegaly – Increase: MCV - macrocytosis • Reticulocytes – IMMUNE: (+) Direct anti-globulin test(Coomb’s) – History of pigmented(Bilirubin) gallstones
hemolytic anemia
HEMOLYTIC ANEMIA – ACQUIRED ETIOLOGIES
IMMUNE (Coomb’s +)
Autoimmune Hemolytic anemia(AIHA) Warm: Idiopathic & CLL Cold: Idiopathic & Mycoplasma Alloimmune: Transfusion Drug-induced
– Antibody or complement on RBC (looking for abs on RBC)
– Diagnosis of:
• AIHA
• Hemolytic transfusion reaction
direct coombs
– 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
– Auto-ATB against RBCs
– Warm & Cold Auto-ATB
AIHA
Any Age Usually IgG Variable anemia Etiologies: 65% - Idiopathic 25% - CLL 20% - NHL Other – Meds Clinical Anemia Jaundice Splenomegaly
warm auto ATB
– IgM – Etiologies: • Idiopathic • Mycoplasma • Lymphoma • Mononucleosis – Clinical • Acrocyanosis at cold temperatures • Jaundice • Splenomegaly
cold auto atb
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
Inherited hemolytic blood disease resulting from a mutation in the alpha globin gene
• Normal HGB = “A1”
• Hemoglobin “S”
Sickle Cell Disease
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
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
sickle cell skeletal presentation
- Marrow hyperplasia=osteopenia=fractures
- “Hair-on-end” on skull
- Marrow infarction = osteonecrosis
- Dactylitis
- Osteonecrosis
- Bossing
– 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
– 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
heinz bodies
excess alpha chains
– Heterozygous carrier – Usually no clinical symptoms – Asymptomatic Splenomegaly 20% – CBC/peripheral smear • Mild anemia(Hct>30) • MCV
B-Thal Minor
• 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
• 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
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
– Silent carrier = (α - / α α) – Trait • Similar to β Thal trait • Mild heme changes • No clinical abnormality
a Thal (silent carrier)
- Mod-severe hemolytic anemia – hypo/micro –retic counts to 15%
- HSM / Gallstones / Leg ulcers
- RBCs contain Hgb H precipitates
– Hgb H Disease (α - / - -)
– Hgb Bart’s (- - / - -) (γ4) =
incompatible with life
other names for myelodysplastic syndromes
– Refractory anemia
• No improvement with Fe / B12 / Folate
– Pre-Leukemia
– Senile anemia
Ringed sideroblasts
myelodysplasia
• 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
myelodysplasia therapies
Bone Marrow Transplant is only curative
– van den Berghe Nature 1974 – severe anemia – mild leukopenia – normal or increased platelets – atypical megakaryocytes – indolent – <5% blasts
5q treatment
5q syndrome
Lenalidomide
Myeloproliferative Disorders
• BCR/ABL(+): Chronic Myelocytic Leukemia
• BCR/ABL(-) & JAK2(+):
– Essential Thrombocythemia
– Myelofibrosis with Myeloid Metaplasia
– Polycythemia rubra vera
• JAK2(+/-): Chronic Myelomonocytic Leukemia
• 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
CML treatment
Imatinib (Gleevec)
•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
• 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
• 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
– Most common neoplasm in
ALL
ALL sites
Marrow usually
ALL presentation
– Bulky adenopathy
– Mediastinal mass
– Pleural effusions
– +/- hyperleukocytosis
ALL Lab
– ↑ WBC or Pancytopenia +/- Blasts
– LDH (= tumor burden)
– Hypercalcemia
– ↑ Uric acid / LFTs / BUN
ALL treatment phases
– Induction
– CNS
– Consolidation
– Maintenance
• 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
• 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
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
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
t(2;5)
t(8;14)
t(14;18)
t(11;14)
ALCL
Burkitts
Follicular
Mantle
– 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
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
• 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
• 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
• 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
- 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
- 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
• 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
• 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
– 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
- Cutaneous T Cell lymphoma
- Multiple cutaneous plaques – nodules
- Generalized erythroderma
- Treatment often topical
Mycosis Fungoides
• 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
- 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`
Typles of plasma cell neoplasms
• Clinically Benign: – MGUS • Indolent: – Waldenstrom’s – Indolent Myeloma • Malignant: Plasma Cell Myeloma • Malignant Aggressive: Plasma Cell Leukemia
• 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
- Monoclonal protein serum a/o urine
2a. Plasmacytoma OR
2b. Marrow plasmacytosis > 10% - CRAB:
• Calcium
• Renal - light chain tub interst nephritis
• Anemia
• Bone - osteoporosis
Rouleax formation
Multiple Myeloma
Myleoma symptoms
back pain headache blurry vision CHF Sausage retinal veins
Collection of plasma cells usually in vertebral body
Solitary Plasmacytoma (treat with bisphosphonates)
virchows triad
– Venous stasis
– Blood vessel damage
– Hypercoagulability
Disorders of Thrombosis -Prophylaxis in Podiatric Surgery
3 significant risk factors
– Prior VTE
– Hormone replacement/Oral Contraception
– Obesity
– 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
- Increase O2 carrying capacity
- Not for volume replacement
- Symptomatic anemia / acute hemorrhage
- Increase HGB in adult ~ 1 GM / DL
Packed RBCs
- Replaces volume and O2 carrying capacity
- <1% of all xfusions
- Large amount of plasma
Whole Blood
- Wash with saline to remove plasma
* Indication – repeated hypersensitivity reactions
Washed RBCs
- Remove WBCs by filtration
* Indication – multiple non-Hemolytic transfusion reactions
Leukoreduced RBCs
– 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
– 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
• 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
– 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
• 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
• Small amount • Sudden onset & rapid progression – Respiratory distress – Vascular collapse – Afebrile • IgE response to transfused proteins • Particularly susceptible IgA deficients
Anaphylactic Reaction
- Noncardiogenic pulmonary edema
- Usually ~ 2 hours after xfusion
- Acute respiratory insufficiency & hypotension
- CXR = bilateral white out
- Fatality 7%
TRALI
Platelets are involved in _________ hemostasis
primary
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
- Intravascular purpura
- Platelet disorders
- <3mm
- Non-palpable
Petachia
thrombocytopenia bone marrow smear
increased cellularity
megakaryocytes
- 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
– 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
• 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
- Children>Adults
- Prior Infection
- vWF protease normal
- MAHA / Thrombocytopenia (< TTP)
- ARF (renal > TTP)
- No Neurologic or Fever
HUS
Platelet Transfusion - Parameters
– 60,000
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
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
– Prolongation: dec in Fs II/V/VII/X/Fibrinogen
– Extrinsic system abnormalities
– INR(Int. Normalized Ratio) for Warfarin patients
Prothrombin Time(PT
Prolongation is dec for factors II/V/VIII/IX/X/XI/XII
– Intrinsic system
– Rarely affected by fibrinogen
aPTT
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)
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
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
Abnormal PT + aPTT
– Coagulopathy of liver disease – Deficiencies of individual factors • Factor II (Prothrombin) • Factor X (Stuart-Prower) • Factor V (Proaccelerin) – DIC – LA
cuases of ataxic gait
posterior column disease
cerebellar degeneration
peripheral neruopathy
Steppage gait causs
LMN disease such as neuropathies (syphillis) Tabes dorsalis
Stiff spinal cord gait - circumduction gait
UMN disease
Magnetic gait
Normal Pressure Hydrocephalus
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
Resting tremor unilateral cogwheel rigidity Bradykinesia asymmetric onset treatment
Parkinsons disease
start with levodop or dop agonist first to control symptoms
Less tremor than parkinsons vertical gaze impaired Stiff gait --Fall backward Axial rigidity, hyperextended Falling is big concern
Progressive supranuclear palsy
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
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
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
acute flares of MS treated with
IV glucocortricoids
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
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
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
Can be Compressive myelopathy
Motor and sensory symptoms
Below level affected
Spinal stenosis
Meylopathy
“Cape-like numbness”,
Symptoms of myelopathy include paraparesis and a sensory level
Intraxial widening of the central canal
Syringomyelia
Pathology of the spinal cord
myelopathy
myelopathy signs and symptoms
Spasticity Upper motor neuron Sensory level Bladder and bowel incontinence Pain Characteristic gait: Stiff and erect (Stiff Man Gait)
A febrile diabetic with back pain and myelopathy has what?
epidural abscess til proven otherwise
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
Confused w/ cellulitis & DVT
Usually post-op
Severe hypersensitivity w/ swelling & sweating
CRPS/RSD/Causalgia
Desire to move legs Feeling of motor restlessness Worse with rest or at night Better with activity dx by history
Restless leg syndrome
Drugs taht cause tremor
beta agonists (sympathomimetics)
Lithium
Antipsychotic
Valproic Acid
Drugs associated with PerNeur
amidoraone
vincristine
metrnidazole
halothane
Vincristine
B-6
INH are the biggies
drugs with myopathis
statins
steroids
accutane
chloroquine
General myopathy symptoms
Painful Myalgias Cramps Contractures Myotonia - Stiff Myoglobinuria No weakness, fatigue, exercise intolerance, muscle atrophy
Boys Absent dystrophin Pseudohypertrophy Positive Gowers sign Cognitive imparitment Waddling gait Cardiac probs High CPK
Duchenne’s
myopathies vs NMJ
NMJ Diseases generally involves proximal muscular weakness and is symmetrical.
See MG and LEMS above
Endocarditis or arrhythmia associate with what stroke
embolic
HTN with what stroke
Lacunar
CAD with what stroke
thrombotic
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
common causes of spasticity
Stroke Cerebral Palsy Traumatic brain injury Anoxia Spinal cord injury MS ALS, PLS, MSA Metabolic diseases (Leukodystrophies)
treatments for spasticity
Benzodiazepines, Baclofen, Tizanadine (Zanaflex) Botox. Also PT, serial casting, orthoses, orthopedic procedures
Unilateral pulsating moderate to severe aggrevated by activity Photo & or phonophobia prodrome -> aura -> HA -> post drome
migraine
types of migraine
common - no aura
classic - aura
complex - focal neuro deficity
basilar - HA, N, vertigo
tx for migraine
non pharm - foods, etoh, caff
acute - nsaids, ergot, steroids, narcotics
preventative - TCA, CCB (2nd) BB, Depakote, botox
Unilateral severe ice pick retroorbital stiffness, rhinorrhea, occur in clusters smoker
cluster
02, steroids, lithium CCB
base of skull to temporal region band like palpable muscle tension stress overlap with migrain 30 min to 7 days pressing or tightening
tension
worst HA of my life
sub-arachnoid hemorrhage
neuro emergency
parkinsonisms frontal visuospatial dementia fluctuating cognition recurrent visual hallucination lang and mem still good
Lewy body dementia
magnentic gait
incontinenc
normal p hydrocephalus
How are peripheral neuropathies classified?
Acute Chronic Motor Sensory Compression Hereditary Axonal – Lower Amplitude Demyelinating – Slower amplitude
myelinopathies types
acute - guillian barre
chronic
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
NM disease
DTR intact
Perioral numbness
dysphagia
botulism
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
Signs and symptoms of osteoporotic fracture
height loss, kyphosis, or unexplained back pain
previous or current facture
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
PTH analog
Teriparatide
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
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
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
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
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
– 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
Cushing’s Diagnosis
– Elevated plasma cortisol
– Dexamethasone suppression test failure
– ACTH may be elevated or low
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
adrenal adenomas are common
t/f
true
• 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)
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
• 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
treatment for addisons
– Hydrocortisone 20-30 mg daily
– Fludrocortisone 0.05-0.1-mg daily
• 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
• Hypovolemic cardiovascular collapse
– Fatal if unrecognized
addisonian crisis
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
– Symptoms • Paroxysmal beta adrenergic symptoms – Laboratory findings • Urinary free catecholamines, VMA, metanephrines – CT scan tumor localization
Pheochromocytoma
treatment for pheochromocytoma
phenoxybenzamine
type 1 DM clinical manifestations
polydipsia polyuria polyphagia Ketosis-prone absolute insulin deficiency
infants and children first manifestation of Type 1 DM
ketoacidosis
type 2 clinical manifestation of type 2
recurrent infections genital pruritis hyperglycemia, visual changes parasthesias and fatigue
effects of hyperglycemia
glycation of proteins (hemoglobin, collagen)
accumulation of sorbitol and fructose (nerves, lens)
activation of protein kinase C (vascular cells)
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
type 1 general treatment
insulin
lifestyle modification
–no glycemic control
General treatment of type 2
diet, exercise, drugs
Glycemic control
Mechanism of action: Decrease hepatic glucose production
Little risk of hypoglycemia;
Lactic acidosis with CHF and renal failure;
Weight neutral
Insulin secretagogues:
metformin
insulin secretagogues names
sulfonylureas (glyburide, glipizide)
repaglinide
nateglinide
Mechanism of action: Increase basal and/or postprandial insulin secretion
Hypoglycemia can happen
Weight gain can happen
Sulfonylureas/glyburide:
Possibly useful before the heaviest meal of the day
Meglitinides/nateglinide
Suppresses appetite;
Weight loss;
Improved insulin sensitivity;
Injectable
GLP-1 agonists/Exanatide:
Oral; similar to GLP-1 agonists but weight neutral
DPP-4 inhibitors/sitagliptin:
Mechanism of action: Enhance tissue response to insulin
Weight gain
CHF risk
long bone fracture risk
TZDs/pioglitazone:
generally start type 2 DM meds with what
metformin and/or a sulfonylurea
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
70/30 dosing
most common insulin regimen
70% NPH and 30% regular
morning dose covers glucose values before dinner
evening covers fasting glusoce
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
basal bolus isulin
basal one dose
bolus based on carbs 1:15 CHO
–short acting
other DM goals
Diabetic LDL <125/70 if nephropathy
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
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
DKA stymptoms but without met acidosis
and diff in treatment
Hyperglycemic Hyperosmolar State
Never give bicarb
most common cause of hypothyroidism
iodine worldwide
hashimotos in developed countries
t4 low
tsh normal
2ry hypothyroidism
tired dry skin cold poor memory constipagtion weight gain t4 low tsh high
hypothryoidism
floppy baby umbilical hernia large tongue neuro damage pericardial effucsion
cretinism
hypothyroid tx
t4 replacement
levothyroxine at 50mcg
wait 3 to 6 weeks to equilibriate
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
graves treatment
beta blockers (propranolol)
sometimes tpo inh
–propylthriuracil, methimazole
average age 60 goiter thyroid lymph infiltrate elevated TSH, low t4, TPO and anti-TG antibodies enlarged cystic nodular thyroid hypothyroid symptoms
hashimotos
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
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
“stones, bones and groans” sually caused by adenoma hypercalcemia hypophospatemia high PTH osteoporosis osteomalcia kidney stones muscle waekness
hyperparathyroidism
“classic” subperiosteal bone resorption with prolonged disease, often involvin phalangeal tufts
– rarely seen in developed countries anymore
Osteitis fibrosa cystica
primary hyperparathyroidism
gold standard for primary hyperparathyroid
surgical treatment
can use calcitrol
vit D
cinacalcet
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
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
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
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
Most common cause – H. Pylori
Duodenal (90%) and gastric ulcers (70%)
PUD
NSAIDs – 2nd
tx
ulcers
antisecretory therapy plus antibiotics
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
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
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
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
But not in place of endoscopy
Will show Stricture, Mass in esophageal cancer and in peptic stricturs
barium swallow
Classic dilated esophagus
Bird’s beak appearance
Due to tight LES
Best seen on Barium Swallow
achalasia
History of Reflux or Barrett’s esophagus
Now has Solid food dysphagia
Weight loss
adenocarcinoma
History of Reflux
Now has Solid food dysphagia
NO weight loss
peptic stricture
History of intermittent dysphagia
Solids, especially breads and meats
No weight loss
Schatzki’s Ring or a Cervical Web
scc of esoph
tobacco and alcohol
women
proximal to mid esop
adenocarcinoma of esoph
barretts
white males
distal esoph/gastric cardia
History of intermittent dysphagia
Liquids or Solids & Liquids
No weight loss
achalasia
If patient has rectal Bleed first check
if orthostatic
may need to give fluids or resescetate
Intermittent Diarrhea without blood Especially young woman May be associated with bloating and abdominal cramps No weight loss Rarely nocturnal diarrhea
IBD
Middle age or eldery Blood mixed with stool Several months Now has lightheadedness Iron Def anemia
how to diagnose
Colon cancer
colonoscopy
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
Any age
Very Short duration of bloody diarrhea
Associated with ab pain and fever
infectious diarrhea
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
Massive bleeding from rectum
History of repaired abdominal aortic aneurysm
Very unstable due to large amount of bleeding
Aorto-enteric fistula
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
Hematemesis
Ab pain
History of being on NSAIDs
May have coffee grounds as well
PUD
History of recurrent non-bloody vomiting followed by bloody vomiting
Mallory Weiss tear
Coffee Ground emesis
History of heartbur
esophagitis
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
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
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
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
Ulcerative colitis and Crohns
Extra-intestinal manifestations
Erythema nodosum Pyoderma gangrenosum Arthritis, Iritis Episcleritis
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
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
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
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
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
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
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
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
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
You want to do an elective procedure on a patient with cirrhosis
t/f
false
hep b vaccinated vs immunity
vaccinated are positive for anti-HBs but not anti-HBc
Immune are positive for both
pharm and elderly
elderly have decrease in hepatic and renal metabolism so may need to decrease those drugs
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
• 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
• 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
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
Chronic impairments of o Cognitive function o Mobility, Dexterity Environmental factors Psychological Factors
Functional incontinence
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
Treatment for Stress inco
behavior therapis
alpha adrenergic
estrogen
surgery*
treatment for urge
behavioral therapies
bladder relaxent drugs
treatment for overflow
surgery
catheterization*
Nearsightedness
Difficulty seeing objects in the distance
myopia
Farsightedness
Difficulty seeing near objects
hyperopia
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
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
Most common cause of blindness in the elderly
Characteristically central blindness
Usually excellent peripheral vision
macular degeneration
Drusen (yellow byproducts of metabolism) accumulate under the macula
dry macular degeneration
Increasing drusen accumulation with angiogenesis and choroidal neovascularization
wet macular deg
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
Characterized by ischemia, neovascularization, microaneurysms and hemorrhage.
Importance of annual ophthalmologic examinations for diabetics
Glycemic and antihypertensive control are both important
diabetic retinopathy
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
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
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
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
- Common
* Thinning skin in an older persons external auditory canal produces thicker, drier and more adherent cerumen
Cerumenosis
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
review rinne / weber
conductive - bone > air (cba)
—-localizes to affected ear
ssn - air > bone
—–localizes to unaffected ear
the pathobiology of alzhiemeirs is characterized by
amylid plaques
neurofibrillary tangles
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
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
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
• 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
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
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
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
spastic hemiparises gait cause
CVA
Scissors gait cause
lower extremity spastic paresis from cervical spondylosis
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
hyponatreamia def
Na < 133
determines intravascular volume
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
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
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
how to correct for hypoalbuminemia in met acidosis
– (Expected albumin – observed albumin) x 2.5 + (observed anion gap) is the
actual anion gap.
metabolic alkalosis causes
»likely diuretics, vomiting, hypokalemia (e.g., aldosteronism)
creatinine and GFR relationship
inversely
Acute Renal Failure causes
- Pre Renal
- Post Renal
- Renal
- Mucous membranes are dry
- Tenting of the skin- Where?
• Thigh and calf - Flat neck veins
- Orthostatics- Laying/Sitting/standing SBP >20 mm Hg fall,DBP>10 mmHg fall, Pulse
increase of >20 - Wait 3 min between each maneuver
Fe Na 20/1 - Volume loss (GI- N-V-D and diuretics)
- Relative Vol Loss (CHF,Cirrhosis, Nephrosis, Pancreatitis, Burns, etc)
- Gastro Intestinal Bleed
- Hypercatabolic state (Prednisone, Sepsis Neoplasia, Burns)
- TPN
Pre-Renal Azotemia
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
Fe Na > 3 Bun/Cr < 15/1 U Na >20 1. No Tenting 2. Normal Membranes 3. Hypotension 4. Could be anything
Renal ARF
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
- Proteinuria (>3.0 Gms/day)… actually albuminuria
- Edema
- Hyperlipidemia ( why?)
Nephrotic syndrome
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 !!!!!!
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
Again, does not reflect Na stores,rather, total body H20 deficit
Sx = Altered mental status why?- brain cells “shrink”
Hypernatremia
hypernatremia treatment
D5W; NOOOOO Salt!!! (e.g., NS, D5 1/2 NS, D5 1/4 NS)
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+
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
treatment for hyperkalemia
Ca Gluconate immediatley
Anion Gap Metabolic Acidosis - MUDPILES
Methanol Uremia DKA Paraldehyde Isopropyl alcohol Lactic Acidosis Ethylene Glycol Salicylates
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
Treatment for met acidosis
Alkalinize urine Cathartic Replace electrolytes Dialysis Bezoar - 35hr peak levels NEVER SEDATE PATIENT
Respiratory Acidosis causes
COPD
End stage ARDS
Iatrogenic
Inability to remove CO2 with ventilation
Turn up O2
Respiratory Alkalosis
Hyperventilation
Causes- Anxiety, Sepsis, Fevers, Gram negative bacteremia, Iatrogenic, Aspirin toxicity
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
4 kinds of kidney stones
calcium - hyperpara,
uric acid - hyperuricemia
cystine
struvite - bacterail enzyme degredation
struvite stone tx
remove stone and antibiotic
- 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
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
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
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
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
• 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
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
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
– 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
• 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
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
Usually an abnormal vaginal discharge and abnormal vaginal bleeding, especially postmenopausal bleeding
Endometrial uterine cancer
how to diagnose and treat
endometrial biopsy
hysterectomy
• Increased risk with multiple sexual partners, likely due to HPV (human papilloma virus)
• Diagnosis
– Pap smear / colposcopy
cervical cancer
most common organism in UTI
e coli
– 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
– Similar to cystitis but may include a vaginal
discharge in females
urethritis caused by chlamydia, gonorrhea and genital herpes
– 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
gold standard to diagnose uti
urine culture
get a UA too
flank pain and intractable vomiting
kidney stone
WBC casts … what is it and what to do
pyelonephritis — need hospital and IV antibiotics to avoid septic shock
Fatty casts
nephrotic syndorme
RBC casts
nephritic syndrome
ideal BP for a diabetic
125/75
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
x-rays rapiopaque and radiolucent
- Radiopaque - Bright
* Radiolucent- Dark
filter used in podiatry
2.5mm total
how many screens used in podiatry
one
controls radiographic contrast.
kvp
kvp and subject contrast
high kvp = lower subject contract
low kvp = high subject contrast
low kvp increases pateint dose
determines the number of x-rays produced
how much used in podiatry
mA
15-30
exposure time
1/60sec
• Patient dose is therefore a function of
mAs
• 15% rule
15% change in KVP is equivalent to 2 times of a change in MA
inversely
Inverse Square Law
• Radiation intensity is inversely proportional to the square of the distance from the source
common source to image distances
40” or 100cm
focal spot sized used in podiatry
1MM
greatest tool in keeping patient exposure as low as possible
Collimation
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
words for bright on xray
Synonyms
Radiopaque
Sclerosis*
Eburnation*
opaque – increase in subject density leads to decrease in optical density. Film appears white.
words for dark on xray
Radiolucent
Rarefaction*
Osteopenia*
Osteolysis*
lucent - black areas on film. A decrease subject density leads to increase in optical
density.
Bone apposition on xray
100% is normal
0% is dislocated
Anything between is subluxed
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
bipartite bones seen
sesamoides
med cun
navicular (rare)
anteater signs
CN coaltion
Sclerotic halo usually with flat foot
TC coalition
os veselanium
off of 5th met base
os peroneum
lateral to cuboid
os eccentric interphalanges
prox lateral distal phalanx of hallux
os naviculare
deeper in TN joint
type II accessory navicular
against navicular but not joint
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)
primary growth centers are all present at birth except
navicular cuboid? lat cun med cun int cun 2ry ossification centers
apophysis vs epiphysis
• Epiphysis – part of bone that develops separately and then ankyloses.
–Common in tubular bones.
• Apophysis – outgrowth or swelling of bone.
–Tuberosity
multiple primary turn into what
bipartites
common locations of a pseudoepiphysis
head of 1st met
bases of 2, 3, 4
TC coaltion usually seen in 2nd decade and
–Anterior facet – MO
–Posterior and middle – calcaneal axial
–“C” sign
–Talar beaking
TN coalition best seen on what view
lateral
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
most commonly used bone scan radionuclides
why use
tech 99
good marker of inflammation
Good for tumor localization and infection
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
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
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
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
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
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)
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)
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.
Metal implants
High grade stainless steel, titanium, metal alloys may cause artifacts to show up on image causing blurred image
muscle on all mri is always
dark grey
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
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.
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
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
- 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
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
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)
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
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)
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
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
ELONGATION & THINNING OF LONG BONES
ARACHNODACTLY
ABNORMAL COLLAGEN
marfans
- 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
- Juxta-articular Cysts
- Juxta-articular
- Erosions
- Joint Subluxation
- Joint Dislocation
- Osteoporosis
- Osteopenia
- osteomyelitis
- Demineralization
RA
- Effusion–Early
- Joint Space Narrowing–Late
- “Punched Out Lesions”
- Overhanging Margins
- Martel’s Sign
Gout
- “Fluffy Heel Spur”
- Ankylosing Spondylitis
- Sacroiliitis
- Vertebral Squaring
- SHINING CORNERS
- Syndesmophytes
- Bony Bridging
- Bamboo Spine
- “Fluffy Heel Spur”
Reactive Reiter’s
- Erosions
- Sacroiliitis
- Terminal Whittling of Proximal Bone
- “Pencil in Cup”
- ARTHRITIS MUTILANS
- Sausage Toe
Psoriatic arthritis
Factors to be considered on all chest x-rays include
Inspiration Penetration Rotation Angulation Orientation
Fluffy upper lobe infiltrates
Could be cocci, but can’t make that diagnose on xray
TB
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
Thin walled cavity think what
Thick
thin - TB, Cocci, WB
Thick -> lung/mass tumor
enlarged heart on cxr, what test do you get next
Echo
could be pericardial effusion or cardiomegaly
pneumothorax treatment
Treatment is to put on O2 or a breathing tube
Recognize if mediastinum is shifted (Tension
SOB, previous DVT
get what test
CT angiography
VQ scan is second but a poor choice
COPD signs on chest x-ray
enlargement of retrosternal space and diaphragm flattening
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?
Contra-Indications to IV Contrast
Iodine Allergy
Renal Failure & Not on Dialysis (Based on BUN/Cr and GFR)
Foreign Bodies imaging choice
ultrasound
Salter Harris Classifications
1 – transverse thru GP 2 – GP and Meta 3 – GP and Epiphysis 4 – GP and Meta and Epiphysis 5 – Crush injury
Fracture from FOOSH from normal height
Refer to orthopedic surgeon
Dexa scan if fragility fracture
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
Acute Appendicitis imaging
US in kids
CT in adults
Gallstones imaging
ultrasound
DVT Dopper things to look for
Compression
Color Flow
Augmentation
metastasis to bone
sclerotic and lytic
Sclerotic: Prostate, Lung, Breast
Lytic: Breast, Lung, Renal Cell, Thyroid, MM
Complications of pagets
Pathological fractures 2ry Osteoarthritis Bony deformities Deafness Spinal Stenosis High output CHF Osteosarcomas
how to differ bakers from dvt
Ultrasound
MR if ruptured
atlanto-axial subluxation seen in what
rheumatoid
avn commonm places
- Femoral Head
- Humerus
- Knee
- Talus
SI involvement bilateral syndesmophytes enthsitis whiskering bamboo spine \
ankylosing spondylitis
asymmetry DIP early widening of joint later narrowing pencil in cup
psoriatic arthritis
grading edema
- 0- no edema present
- 1- mild
- 2- moderate
- 3-moderate to severe
- 4-severe
• Valleix Phenomenon
– Percussion of the nerve causing proximal and distal radiation or paresthesias
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
inflammation of vein with blood clot (thrombus) formation (superficial &
deep
thrombophlebitis
painless, insidious swelling of the Tissues leadiang to decreased function of the
lymphatic system. May be congenital or acquired
lymphedema
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
Class I synovial fluid findings
Clear/yellow Transparent WBC < 2,000 <25% pMNs Culture negative
ClassII Synovial findings
Yellow/White Translucent/opaque WBC 2,k to 100k > 50%pMNs culture neg
Class III synovial findings
yellow/white Opaque > 100k WBC > 95% PMNs Culture positive
Class IV synovial findings
Red
Opaque
physical findings of OA
firm swelling around joint
crepitus
restricted ROM
OA common joints
hips knees 1st carpal metacarpal joint 1st MTP PIP, DIP
RA common joints
wrists
MCP
ankles
MTP
lab tests for RA
high ESR high CRP' post rf pos ccp anemia
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
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
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
Foreign body sensation (sandy or gritty) Dry or decreased tearing Burning Photosensitivity Itching Filmy sensation
sjogrens syndrome
RA Splenomegaly Neutropenia Other Features Anemia Thrombocytopenia Lymphadenopathy Leg Ulcers Skin Pigmentation
Felty Syndrome
5 clinical syndromes of Psoriatic arthritis
Asymmetric oligoarticular Symmetric polyarticular Arthritis Mutilans DIP Only Axial Skeleton
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
treatment for asymptomatic hyperuricemia
nothing
uricosurics
probenicid
xanthine oxidase inh
allopurinol (start at 100)
Feuxostat - hepatic glucoronidation
40mg start
PMales over 60 Knee chondrocalcinosis often degenerative Crystalls CPPD Small rod like positive birefringence
pseudogout
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
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
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
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
diabetic complications
heart disease
blindness
kidney disease
amputation
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
pedal complications in diabetes
Neuropathy Vasculopathy Immunopathy Limited Joint Motion Ulcerationi Infection Gangrene Charcot Collapse
unholy triad
Neuropathy….….loss of sensation to extremities
Vasculopathy …..decreased blood flow
Immunopathy…..inability to fight infection
risk stratification for diabetics
0 - normal - q12 m
1 - PN - q6 m
2 - LOPS, deformity, PAD, q3m
3 - Previous ulcer or amp q1-3m
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
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
- ‘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
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
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
= Rapidly reversible sensory symptoms in poorly controlled diabetic patients during episodes of elevated blood sugar.
hyperglycemic neuropathy
= Asymptomatic neuropathy becomes temporarily symptomatic with rapid drop in blood sugar
“Insulin Neuritis”
PN best prevention tool
normoglycemia
therapeutic options for PN
•Symptom Relieving Only ▫ Physical modalities ▫ Antidepressants ▫ Anticonvulsants •Disease Modifying ▫ Intensive glucose management ▫ Antioxidants/nutriceuticals ▫ Decompression
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)
Major predisposing factor for DFI is
DF ulcer
evidence of infection in DFU
Redness, warmth, swelling, tenderness, or pain
Purulent secretions, undermining of skin edges, foul odor
Factors that increase risk of infection:
Probe-to-bone test +, >30 days, recurrent ulcer, PVD
LOPS, renal insufficiency, barefoot walker
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.
• 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
- 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
• 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
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
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
avoid prescribing antibiotic for what
uninfected ulcers
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
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.
if patient had MRSA in past…..
treat them for MRSA
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
IDSA indication for soft tissue infections with oral meds
2-4 weeks of oral antibiotics.
For osteomyelitis: up to 3 months combined therapy.
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.
mild Staph aurues infection
Keflex
Augmentin (amox/clav)
Clinda
mild MRSA infection
Doxycycline
Bactrim
moderate staph infection
ampicillin-sulbactam
ertapenem
imipenem
moderate to severe MRSA
Vancomycin
Linezolid
Daptomycin
Pseudomona infection
mild - quinolones
mod - Pipercillin tazobactam (zosyn) (broad)
definitive diagnosis of osteomyelitis
bone biopsy
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
Classic periwound signs Brawny edema Hyperpigmentation Lipodermatosclerosis Located in the gaiter (supramalleolar) region Irregular borders Copious drainage Beefy red base Painful
venous ulcers
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
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
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
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
Abrupt appearance Acral location (Acral = away from central trunk) Porphyrin levels Immunoflourescence Intraepidermal Subepidermal no hx of trauma
bullosis diabeticorum
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
May be hemorrhagic Non-inflammed base Tips of toes & fingers, NWB Areas Heals with scarringand atrophy NO HISTORYOF TRAUMA
subepidermal blisters of bulldiab
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)
considerations for Necrobiosis Lipoidica
malignant transformation (biopsy it) biopsy
treatment of NLD
topical steroids
intralesional steroids
