Internal Medicine Review

Tao Zhan, MD
The First Hospital of Changsha
Respiratory Medicine: pneumonia
Classification

• Etiological/Microbiological Classification

• Anatomical/Radiological Classification

• Combined Clinical Classification

Anatomical/Radiological classification

Lobar pneumonia

Interstitial pneumonia
Etiological/Microbiological classification

• Infection with bacteria, viruses, fungi, or parasites

• Chemical or physical injury to the lungs

• Immunological Injury

• Unknown causes
Combined clinical classification

• Community-acquired pneumonia (CAP)

• Hospital-acquired pneumonia (HAP)

--Ventilator associated pneumonia (VAP)

• Healthcare-associated pneumonia (HCAP)

• Immunocompromised host pneumonia (ICHP)

 Clinical Diagnosis

Which one is the Most Wanted ?

Any relevant symptom or sign+radiological evidence

Clinical Diagnosis

Exclude TB, Ca, non-infectious interstitial diseases, pulmonary e

dema, atelectasis, embolism, eosinocyte infiltration and vasculi
tis, etc.

Exclude Every Disease That Can Mimic Pneumonia before Diag

nosis Established
 Community-acquired pneumonia
CAP

• infectious pneumonia in a person who has not recentl

y been hospitalized

• most common type of pneumonia

 Community-acquired pneumonia
CAP

Pathogen Prevalence （ % ）
S pneumoniae （肺炎链球菌）
20–60
H influenzae （流感嗜血杆菌）
3–10
Oral anaerobes （口腔厌氧菌）
6–10
S aureus （金黄色葡萄球菌）
3–5
Other Gram-negative bacteria （其他革兰阴性菌） 3–10
Respiratory viruses （呼吸道病毒） 2
–15
L pneumophila （嗜肺军团菌）
 Initial empiric therapy for suspected CAP
outpatient: previously healthy

• No recent antibiotic therapy

A macrolide( 大环内酯 ) or doxycycline ( 多西环素 )

• Recent antibiotic therapy

A respiratory fluoroquinolone ( 呼吸氟喹诺酮 ) alone

An advanced macrolide ( 大环内酯 ) plus high-dose amoxicillin ( 阿莫西林 )
An advanced macrolide ( 大环内酯 ) plus high-dose amoxicillin-clavulanate ( 阿莫西林 / 克拉维酸 )
 Initial empiric therapy for suspected CAP
outpatient: comorbidities

• No recent antibiotic therapy

An advanced macrolide( 大环内酯 ) or a respiratory fluoroquinolone ( 呼吸氟喹诺酮 )

• Recent antibiotic therapy

A respiratory fluoroquinolone ( 呼吸氟喹诺酮 ) alone or an advanced macrolide ( 大环内酯 ) plus β-lact
am (β 内酰胺类 )

• Suspected aspiration with infection

Amoxicillin-clavulanate ( 阿莫西林 / 克拉维酸 ) or clindamycin( 克林霉素 )

• Influenza with bacterial superinfection ( 细菌二重感染 )

A β -lactam (β 内酰胺类 ) or a respiratory fluoroquinolone( 呼吸氟喹诺酮 )
 Initial empiric therapy for suspected CAP
Inpatient

• No recent antibiotic therapy

A respiratory fluoroquinolone( 呼吸氟喹诺酮 ) alone or an advanced macrolide
( 大环内酯 ) plus a b-lactam (β 内酰胺类 )

• Recent antibiotic therapy

An advanced macrolide ( 大环内酯 ) plus a b-lactam (β 内酰胺类 ) or a respirator
y fluoroquinolone( 呼吸氟喹诺酮 ) alone (regimen selected will depend on natur
e of recent antibiotic therapy)
 Initial empiric therapy for suspected CAP
ICU
• Pseudomonas infection is not an issue
A b-lactam plus either an advanced macrolide or a respiratory fluoroquinolone

• Pseudomonas infection is not an issue but patient has a b-lactam allergy

A respiratory fluoroquinolone, with or without clindamycin

• Pseudomonas infection is an issue

(1) an antipseudomonal agent plus ciprofloxacin( 环丙沙星 )

(2) an antipseudomonal agent plus an aminoglycoside plus a respiratory fluoroquinolone or a macrolide

• Pseudomonas infection is an issue but the patient has a b-lactam allergy

(1) aztreonam( 氨曲南 ) plus levofloxacin( 左氧氟沙星 )

(2) aztreonam plus moxifloxacin( 莫西沙星 ) or gatifloxacin( 格替沙星 ), with or without an

aminoglycoside( 氨基糖苷类 )
Respiratory Medicine: asthma
 What Is Asthma?

Asthma is a disease that characterized by:

Airway obstruction that is reversible either spontaneously or
with treatment
chronic airway inflammation
Increased airway responsiveness to a variety of stimuli
Inflammation causes recurrent episodes of wheezing, breathl
essness, chest tightness and coughing, particularly at night or
early morning
Did You Know..
Asthma kills people equally regardless of s
everity level
1/3 of deaths are in those with mild asth
ma
1/3 of deaths are in those with moderate
asthma
1/3 of deaths are in those with severe ast
hma
Common Allergens (Triggers)
 SeasonalPollens
 Animal dander saliva/
urine
 Dust Mites
 Cockroaches/Mice/Rat
droppings and urine
 Mold
 Some medications
 Some Foods
Common Irritants (Triggers)
Exercise Chemical irritants a
Cold Air nd strong smells
Chalk Dust Strong emotional fe
Viral/upper respirat elings
ory infections Diesel fumes
Air pollution
Cleaning supplies
Tobacco smoke or s
econdhand smoke
Airway Obstruction

Copyright 3M Pharmaceuticals 2004

Common Symptoms Of Asthma
Frequent cough, especially at night
Shortness of breath or rapid breathing
Chest tightness
Chest pain
Wheezing
Fatigue
Initial Assessment & Diagnosis of Asthma

Determines That:
Patient has a history or presence of episodic symp
toms of airflow obstruction
Airflow obstruction is at least partially reversible

Alternative diagnoses are excluded

Methods for Establishing Diagnosis

Detailed medical history

Physical exam: wheeze and rhonchus (r
honchi)
Spirometry to demonstrate reversibility
 Is Airflow Obstruction At Least Partially Rever
sible?
Use spirometry to establish airflow obstruction
 FEV1 < 80% of predicted
 FEV1/FVC <70%

Use spirometry to establish reversibility

 FEV1 increases >15% and at least 200 mL after using a short-a
cting inhaled beta2-agonist
 Goals Of Asthma Therapy
Prevent chronic and troublesome symptoms

Maintain “normal” pulmonary function

Maintain normal activity levels-including exercise and ot

her physical activity
Minimize the need for emergency room/urgent care visi
ts or hospitalizations
 Goals Of Asthma Therapy
Continued…
Prevent recurrent exacerbations of symptoms

Provide optimal pharmacotherapy with minimal or no

adverse effects
Satisfy the patient’s and the family’s goals for asth
ma care
 Stepwise Approach To Asthma Therapy
Outcome: Outcome:
Control of Asthma Best Possible Results

Controller:
 Daily inhaled

corticosteroid
Controller:  Daily long acting
 Daily inhaled
 When controlled,
bronchodilator reduce therapy
Controller: corticosteroid  Daily/alternate day
 Monitor
 Daily long acting
 One daily medication oral corticosteroid
bronchodilator
 Possibly add long
 Anti-leukotriene
acting bronchodilator
 Anti-leukotrienes
Reliever: Reliever: Reliever:
 Inhaled beta agonist Reliever:  Inhaled beta agonist prn  Inhaled beta agonist prn
 Inhaled beta agonist prn
prn
PEF: ≥80% PEF: ≥80% PEF: 60-80% PEF: <60%

STEP 1: STEP 2: STEP 3: STEP 4:

Intermittent Mild Persistent Moderate Persistent Severe Persistent Stepdown
Repiratory Medicine: COPD
Chronic Obstructive Pulmonary Disease

• Two distinct processes are involved, most often in combination.

• Chronic Bronchitis – dx on history
• Emphysema – dx previously on histology, nowadays clinically (good cli
nical-pathologic-radiologic correlation)
Def: Chronic Bronchitis
• Excessive tracheobronchial mucus production sufficient to cause cough with e
xpectoration for most days of at least 3 months of the year for 2 consecutive y
ears.
• Classification:
1. Simple chronic bronchitis
2. Chronic mucopurulent bronchitis
3. Chronic bronchitis with obstruction
4. Chronic bronchitis with obstruction and airway hyperreactivity.
Def: Emphysema
• Permanent abnormal distention of air spaces distal to the terminal bronchiole
with destruction of alveolar septa (containing alveolar capillaries) and attachm
ents to the bronchial walls.
• Classification:
1. Centriacinar ( centrilobular) emphysema
2. Panacinar emphysema
3. Paraseptal emphysema
4. Senile emphysema
Def: COPD

• Chronic obstruction to airflow due to chronic bronchitis and/or emphy

sema.
• Degree of obstruction may be less when the patient is free from respir
atory infection and may improve with bronchodilator drugs
• Significant obstruction is always present
Spirometric classification of COPD severity us
ing post-bronchodilator FeV1
• Stage I (Mild): FeV1/FVC <0.7; FeV1 80% of predicted
• Stage II (Moderate): FeV1/FVC <0.7; FeV1 50- <80% of predicted
• Stage III (Severe): FeV1/FVC <0.7; FeV1 30-<50%
• Stage IV (Very severe): FeV1/FVC <0.7; FeV1 <30% or <50% but chroni
c respiratory failure is present. (GOLD 2007)
Goals of management
• Recognition of disease (early Diagnosis and staging)
• Smoking cessation (secondary prevention) nicotine replacement and Zyban
• Improvement of breathlessness (Rx of airflow obstruction- bronchodilator drugs)
1.Methylxanthines
2.Short and long-acting B2adrenergic agonists ( incidence of pneumonia with ICS
and LABA combinations)
3.Short and long-acting Anticholinergics- BD of choice in COPD
Gastroenterology: GI bleeding
Causes of Upper GI Bleed
• 1) Peptic ulcer disease - most common
cause
A) duodenal ulcers 29%
will rebleed in 10% of cases within
24-48h
B) gastric ulcers 16%
more likely to rebleed
C) stomal ulcers <5%
Causes of Upper GI Bleed
• 2) Erosive gastritis, esophagitis, duodenitis
some causes are ETOH, ASA, NSAID’s
• 3) Esophageal and gastric varices
causes by portal hypertension
• 4) Mallory-Weiss syndrome – longitudinal
mucosal tear in the cardioesophageal
region
caused by repeated retching
Causes of Upper GI Bleed
• 5) stress ulcers
• 6) arteriovenous malformation
• 7) malignancy
• 8) aortoenteric fistula
Causes of Lower GI Bleeding
• 1) Hemorrhoids - most common cause
• 2) Diverticulosis – common, painless,
and can be massive
Caused from an erosion into a
penetrating artery from the
diverticulum.
• 3) Arteriovenous malformations – common
and seen in people with hypertension and
aortic stenosis
Causes of Lower GI Bleeding
• 4) CA/polyps
• 5) inflammatory bowel disease
• 6) infectious gastroenteritis
• 7) Meckel diverticulum
Diagnosis
• Questions to ask in history
• Any hematemesis, coffee-ground emesis, melena, or hematochezia.
• Any weight loss or changes in bowel habits.
• Any vomiting and retching.
• Any history aortic graft.
• Any history of ASA, NSAID’s, steroids.
• Any ETOH abuse.
• Any history of iron or bismuth which can simulate melena and beets which can si
mulate hematochezia. Note stool guaiac testing will be negative.
Diagnosis
Physical exam
• Vital signs may show hypotension and tachycardia.
• Cool, clammy skin then in shock.
• Spider angiomata, palmer erythema, jaundice, and gynecomastia see
n in liver disease.
• Petechiae and purpura seen in coagulopathy.
• Careful ENT exam to rule out causes that can mimic upper GI bleeds.
• Proper abdominal exam and rectal exam.
Diagnosis
Lab
• CBC
• Electrolytes
• Glucose
• BUN/Creatine –BUN will be elevated in upper GI bleeds
• Coagulation studies
• Liver function studies
• Type and cross-match
Diagnosis
Lab
• CBC
• Electrolytes
• Glucose
• BUN/Creatine –BUN will be elevated in upper GI bleeds
• Coagulation studies
• Liver function studies
• Type and cross-match
Treatment
• Large-bore intravenous lines with fluid replacement.
• Class I + II hemorrhage replace with crystalloid.
• Class III + IV hemorrhage replace with crystalloid and blood.
• NG tube should be placed and can determine upper GI from lower GI
but not 100%. Also NG tubes will not worsen varice bleeds.
• Foley catheter for hypotension patients to monitor output.
Treatment
• Proton-pump inhibitor
• Endoscopy
• Somatostatin, octretide for varices
• Balloon tamponade
• Surgery
• Must get early consultation with gastroenterologist and general surge
on for significant GI bleeds.
Several ways to determine H. pylori infection

• 1) invasive
a) during endoscopy a rapid urease test, histologic
study, or culture can be done.
• 2) noninvasive
a) serologic studies which can not be done as a
follow up for cure due to antibodies being
positive for several years after eradication of
infection.
b) urea breath test can be used to confirm cure.
c) stool antigens test can also be used to confirm
cure.
Gastroenterology: IBD
 Definition

Chronic autoimmune inflammatory disorders, involving some

or all layers of the gut wall.

Ulcerative Colitis (UC) Crohn’s Disease (CD)

Mucosal / submucosal only All layers of wall at risk
 Endoscopic Appearance
Ulcerative Coli Crohn’s Diseas
tis e

Friability
Exudate Cobblestoning
bleeding
Normal colon

Diffuse Focal
ulceration ulceration
 Pathogenesis
Anti-inflammatory
IL-4 / IL-13
IL-1Ra
TGFb
IL-10
PGE2
Pro-inflammatory
TNF
IL-1b
IL-12 / IL-18
IFNg
Ulcerative Colitis vs Crohn’s Dise
ase

10

Ulcerative Colitis
Crohn's Disease
50
40 Indeterminate Colitis
 Symptoms

Ulcerative Colitis Crohn’s Disease

Rectal bleeding
Fecal urgency / tenesmus
Diarrhea (bloody)
Lower abdominal cramping
Diarrhea (non-bloody)
Weight loss
Fever
Perianal drainage/pus
Right lower quadrant pain
 Disease Distribution

Ulcerative Colitis Crohn’s Disease

Anywhere from “mouth to anus”
Rectum  Cecum
Segmental / Skip Lesions
Confluent / Contiguous
Rectum usually spared
Ileal involvement uncommon Ileal involvement common

No perianal disease Perianal disease common

 Ulcerative Colitis – distribution
30% 40% 30%

Mild Severe
Crohn’s Disease – distribution
 Extraintestinal IBD

Eyes
Eyes
Mouth
Mouth Heart
Heart

Liver
Liver Joints
Joints

Blood
Blood
Skin
Skin
 Treatment
Conventional therapies:
 5-ASA/SASP
 Corticosteroids/Budesonide
 Immunomodulators
 Antibiotics
 Anti-metabolites
 Biologic Modifiers
 Prognosis
Ulcerative colitis Crohn Disease

80% have intermittent attacks of their Over a 4-year, 22% of patients remain in

disease remission, 25% experience active

From 10% to 15% of patients pursue a symptoms, and 53% between active and
chronic continuous course inactive disease.
The risk of colorectal cancer in Crohn's

disease above the general population as

high as 26.6
Nephrology: nephrotic syndrome
 Diagnosis:
Pro ++++

• Proteinuria: >3.5g/d
• Hypoalbuminemia: SAlb <30g/L
• Edema
• Hyperlipidemia
Proteinuria (albuminuria)

Figure 3.
 Hypoalbuminemia
• Albumin
• Immunoglobulins
• Metal binding proteins
• Erythropoietin urinary loss
• Transferrin
• Complement deficiency
• Coagulation components
 Hyperlipidemia
• Most NS patients have elevated levels of total and low-density lipopro
tein (LDL) cholesterol with low or normal high-density lipoprotein (HD
L) cholesterol . Lipoprotein (a) [Lp(a)] levels are elevated as well.

• Nephrotic patients often have a hypercoagulable state and are predis

posed to deep vein thrombophlebitis, pulmonary emboli, and renal v
ein thrombosis.
 Mechanisms of Hyperlipidemia

• Increased hepatic synthesis of LDL, VLDL and lipoprotein (a) in respon

se to hypoalbuminemia

• Urinary loss of HDL

• Enzymatic changes with abnormal lipid biosythesis and degradation

 Edema
Two different major mechanisms:
• In the classic theory, proteinuria leads to hypoalbumin
emia, a low plasma oncotic pressure, and intravascula
r volume depletion.
• Subequent underperfusion of the kidney stimulates t
he priming of sodium-retentive hormonal systems suc
h as the RAS axis, causing increased renal sodium and
volume retention.
Edema
 Pathology
• Minimal change disease (MCD)
• Mesangial proliferative glomerulonephritis (MsPGN)
• Membranoproliferative glomerulonephritis (MPGN)
• Membranous nephropathy (MN)
• Focal segmental glomerulosclerosis (FsGs)
 Complications
• Infection
malnutrition
loss of immunoglobulins
corticosteroids

• Thrombosis
coagulation, corticosteroids, PLT activity
 Complications
• Acute renal failure (ARF)
Hypoalbuminemia Hypovolemia pre-renal
azotemia

• Protein malnutrition and dyslipidemia

 Diagnosis
• Diagnosis:
NS ?
Primary or secondary ?
Pathological type?
Complications ?
 Differential diagnosis
Type Children Young patients Middle and old age
Primary MCD MsPGN MN
MCD
FsGs
MPGN
Secondary Henoch-Schonlein Lupus nephritis Diabetic
purpura nephropathy
Hepatitis B Henoch-Schonlein Amyloidosis
associated GN purpura

Lupus nephritis Hepatitis B associated Myeloma

GN
Lymphoma and
other tumor
 Treatment
Support care
• Rest; restrict protein intake (0.8-1.0g/kg/d); low salt intake (<3g/d)

• Diuretic therapy

• Diminishing proteinuria: ACEI and ARB

 Treatment

Immunosupressive treatment
• Corticosteroid
Principle of using steroids: start with enough dose (1mg/kg/d), slow
dose tapering (10% every 2-3 weeks), long-term maintenance.

Be careful of side effects of corticosteroid.

 Treatment
Cytotoxic drugs:

•Cyclophosphamide (CTX)

•Cyclosporine (CsA)

•Mycophenolate mofetil (MMF)

 Treatment
• Minimal change disease: sensitive to steroids; single drug; reuse when
relapse; combined with cytotoxic drugs when resistant or dependent
on steroids
• Membranous nephropathy: combine steroid with CTX or cyclosporin/
FK506; avoid when Scr>354umol/L; treat high risk patients with immu
nosuppressive drug immediately.
 Treatment
• Focal segmental glomerulosclerosis: sensitive to steroids in 30-50% of
patients; slow response to therapy; steroids therapy for 3-4 months; if
no response try cyclosporine.
• Membranoproliferative glomerulonephritis: only few adults will respo
nse to steroids.
Nephrology: Urinary Tract Infection
 Classification of UTIs （ 1 ）
Anatomic
 Lower UTI:
 urethritis
 cystitis
(mucosal infectio
n)
 Upper UTI:
 pyelonephritis
 prostatitis
 intrarenal and
perinephric ab
scesses
(tissue invasion)
 Classification of UTIs （ 2 ）
Clinical
 Uncomplicated UTI:
– Lack structural or functional abnormalities of th
e urinary tract
– Normal flow of urine
– NO interference with the normal defenses

 Complicated UTI:
– Predisposing lesion of the urinary tract, structur
al or functional abnormalities, e.g. congenital ab
normality of the urinary tract, stone, obstruction
, catheter….
1. Interference with the normal defenses, e.g. imm
unosuppression, renal disease, or diabetes.
 Classification of UTIs （ 3 ）
Epidemiology
 Catheter-associated （ nosocomial ） infections
:
l Symptomatic
l Asymptomtic

 Non Catheter-associated （ community-acquire

d ） infections:
l Symptomatic
1. Asymptomtic
 Route of Infection
•Ascending route (the most common)

Colonization of urethra
 Etiology （ 1 ）
Community-Acquired UTI
gram-negative bacilli is the most common agent

E. coli

Enterobacter

E. coli Enterococcus

Proteus
Staphylococcus
Klebsiella
 Etiology （ 2 ）
Causative organisms:
Escherichia coli

Klebsiella, proteus and pseudomonas

1- Bacteria S. aureus, Staphylococcus epidermidis and S. saprophyticus

Enterococci (Streptococcus faecalis 粪链球菌 )

Mycobacterium tuberculosis

Chlamydia trachomatis, Neisseria gonorrhoeae

2- Virus Herpes simplex virus , HIV

3- Fungus Candida, Histoplasma capsulatum

4- Protozoon Trichomonas vaginalis, Schistoma haematobium

Clinical presentation （ 1 ）
Cystitis
Burning pain
Frequency, urgency
Suprapubic pain
Dysuria
 Clinical presentation （ 2 ）

Urethritis
Burning pain
Frequency, urgency
Dysuria
Infected with sexually transmitted pathogens
 Clinical presentation （ 3 ）
Acute Pyelonephritis
All cystitis symptoms （ + ） or
（-）
Fever, shaking chills
Nausea, vomiting, diarrhea
Tachycardia, hypotention
Muscle tenderness
Costovertebral angle （ CVA ） pain
Gram-negative sepsis , Leukocytosis
Leukocyte casts in the urine
 Clinical presentation （ 4 ）

Catheter-Associated UTIs
 Bacteriuria develops in at least 10 to 15% of
hospitalized patients with indwelling urethral
catheters.
 The risk of infection is 3 to 5% per day of
catheterization.
 Many infecting bacteria display markedly
great antimicrobial resistance.
 Diagnosis
How is it diagnosed?
•Patient history
•Complete physical examination
•Urine culture
•Urine analysis
•Other examinations
 Diagnosis

Urine Culture Test

(very important)

•Clean urine culture: bacterial counts > 105 /ml

•Suprapubic puncture, catheter collected urine > 102/ml

•Significant bacteriuria
• Microscopic bacteriuria
 Acute uncomplicated cystitis
Pathogens

• Staphylococcus saprophyticus (5-15%)

• Enterobacteriaceae
E. coli (86%)
Klebsiella pneumoniae
Proteus
• Enterococcus
 Acute uncomplicated cystitis
Treatment -- Antibiotic Therapy
• Single-dose therapy is less effective
 Especially with β-lactams
• 3-day course recommended
 TMP-SMX, fluoroquinolone, nitrofurantoin
 NOT appropriate for male patients and complicated UTIs
• 7-day course: Diabetes , age > 65 years, Males
• If untreated: may lead to acute uncomplicated
pyelonephritis treatment
Acute uncomplicated pyelonephritis
Pathogens
• Enterobacteriaceae
E. coli
Klebsiella pneumoniae
Proteus
• Staphylococcus saprophyticus
Acute uncomplicated pyelonephritis
Treatment ( 7–14 days)
• Mild or moderate symptoms:
• Outpatient treatment ( 7–14 days)
• Oral treatment: Fluoroquinolone, TMP/SMX, third gen
eration cephalosporin
• Severe ill patient:
• Hospitalization required
• Parenteral therapy (14 days)
• Broad-spectrum cephalosporins or Fluoroquinolones
 Complicated UTIs
Treatment
• Minimal or mild symptoms (10-14d).
Oral therapy: fluoroquinolone (ciprofloxacin or ofloxacin)

• Severe ill patient, parenteral therapy (10-21d).

Hospitalization required, Imipenem alone
Penicillin or cephalosporin plus aminoglycoside
 Third generation cephalosporin: Ceftriaxone or ceftazidime
 UTI in Pregnant women
Treatment
•Low urinary tract infection (acute cystitis) :
 7 days course antibiotics
 Amoxicillin, cephalosporine, nitrofurantoin
•Pyelonephritis:
 2-4 weeks course antibiotics
 Cephalosporins, extended spectrum penicillins
 Parenteral treatment
 Follow-up urine culture tests, monthly
 Low-dose prophylaxis to recurrent infections
•Asymptomatic bacteriuria
 Antibiotics treatments are needed.
 UTI in catheterized patients
Treatment
• For bacteriuria in asymptomatic catheterized patient:
Catheter removed as soon as possible.
The bacteriuria should be ignored.
• If becomes symptomatic:
Remove catheter
Treatment as described for complicated infections
If the catheter cannot be removed, antibiotic therapy usual
ly proves to be unsuccessful.
Reumatology: SLE
SLE
• Autoimmune disease that affects multisystems
• 1.5 million cases of lupus
• Prevalence of 17 to 48 per 100,000 population
• Women > Men --- 9:1 ratio
• 90% cases are women
• African Americans > Whites
• Onset usually between ages of 15 and 45 years, but
• Can occur in childhood or later in life
Widely Used Criteria by ACR
1. Butterfly rash 7. Neurologic d/o
2. Discoid lupus 8. Hematologic d/o
3. Photosensitivity 9. Renal d/o
4. Oral ulcers 10.Immunologic: anti-DNA
5. Arthritis , anti-Sm, false pos STS
6. Serositis 11.Anti-nuclear antibody
Reminders about the ACR Criteria
• For the purpose of identifying patients in clinical studi
es, a person has SLE if 4 or more of the 11 criteria are
present, serially or simultaneously, during any interval
of observation. (specificity 95%, sensitivity 75%)
• It is important to remember that a patient may have S
LE and not have 4 criteria.
Cutaneous
• Most common rash is photosensitive, raised erythema
tous malar rash. 55-85% develop at some point in dise
ase
• Discoid Lupus Erythematosus (DLE): 15-30% circular, s
caly hyperpimented lesions with erythematous rim, at
rophic center—can be disfiguring
• Mouth/vaginal/nasal ulcers
• Alopecia: may be diffuse or patchy. Occurs 50%
Malar Rash
Discoid Rash
Oral Ulcers
MSK
• Polyarthritis, mild to disabling, occurs most frequently
in hands, wrists, knees. Occurs 90%
• Joint deformities occur in only 10%
• Arthritis of SLE tends to be transitory
• If single joint has persistent pain, consider osteonecro
sis (prevalence increased in SLE over general populati
on, especially if on steroids.)
• Myositis with elevated CK and weakness rarely occurs
Serositis - Pulmonary
• Pleuritis with or without effusion
- if case is mild, tx: NSAIDS
- if case is severe, tx: steroids
• Life-threatening manifestations: interstitial inflammati
on which can lead to fibrosis and intra-alveolar hemor
rhage.
• Also pneumothorax and pulmonary HTN can occur
Serositis – Cardiac
• Pericarditis: most common cardiac manifestation and
usually responds to NSAIDs.
• Myocarditis (rare) and fibrinous endocarditis (Libman-
Sacks) may occur. Steroids plus treatment for CHF/arr
hythmia or embolic events.
• MI due to atherosclerosis can occur in <35 y/o
Neuro
• Cranial or peripheral neuropathy occurs in 10-15%, it is pr
obably secondary to vasculitis in small arteries supplying
nerves.
• Diffuse CNS dysfunction: memory and reasoning difficulty
• Headache: if excruciating, often indicate acute flare
• Seizures of any type
• Psychosis: must distinguish from steroid-induced psychosi
s (occurs in 1st weeks of tx at doses ≥40mg prednisone an
d resolves after several days of reducing or stopping tx)
Neuro
• TIA, Stroke: mostly increased among patients that are
APLA positive
• 50-fold increase in risk of vascular events in women u
nder 45 compared to healthy women
• Treatment for clotting event is long-term anticoagulati
on
Heme
• Anemia: usually Normochromic, normocytic
• Leukopenia: almost always consists of lymphopenia, n
ot granulocytopenia
• Thrombocytopenia
Renal
• Nephritis: usually asymptomatic, so always check UA i
f patient has known or suspected SLE
• Occurs early in course of disease-if not present w/in 1
yr, probably will not occur.
• Histologic classification by renal biopsy is useful to pla
n therapy
Immunoglobulins
• Anti-dsDNA IgG: very specific, may correlate with dise
ase activity
• Anti-Sm: specific, but only present in 25% of cases, do
es not correlate with activity
• APLA: not specific. Used to identify patients at increas
ed risk for clots, thrombocytopenia and fetal loss
ANA
• ANA: positive in 95% of cases. Pretest probability affec
ts interpretation. In PCP setting, 2% for SLE. In rheum:
30%
• Low Positive (1:160 or lower): SLE likelihood <2% (<26
% for rheumatologists)
• High Positive (1:320 or higher): SLE likelihood: 2-17%
(32-81% for rheumatologists)
• SLE specific patterns: Rim and Homogenous
Treatment
• Treatment plans are based on patient age, sex, health,
symptoms, and lifestyle
• Goals of treatment are to:
-prevent flares
-treat flares when they occur
-minimize organ damage and complications
Conservative management
• For those w/out major organ involvement.
• NSAIDs: to control pain, swelling, and fever
• Caution w/ NSAIDS though. SLE pts are at increased ri
sk for aseptic meningitis
• Antimalarials: Generally to treat fatigue joint pain, ski
n rashes, and inflammation of the lungs
• Commonly used: Hydroxycholorquine
• Used alone or in combination with other drugs
Steroids
• Corticosteroids (Mainstay of SLE treatment)
• To rapidly suppress inflammation
• Usually start with high-dose IV pulse and convert to P
O steroids with goal of tapering and converting to so
mething else.
• Commonly used: prednisone, hydrocortisone, methyl
prednisolone, and dexamethasone
Immunosuppressives
• Primarily for CNS/renal involvement
• Mycophenolate mofetil (cellcept)
• Azathioprine (imuran): requires several months to be effective,
effective in smaller percentage of patients
• MTX: for treatment of dermatitis and arthritis, not life-threateni
ng disease
• Cyclosporine: used in steroid-resistant SLE, risk of nephrotoxicit
y
• Cyclophosphamide (cytoxan) Almost all trials performed on pati
ents with nephritis
Additional work-up
 Serum cr. and albumin
 CBC
 Urine Albumin
 ESR
 Complement levels
 Renal biopsy if warranted
Neurology: cerebrovascular diseases
 Definition

• CVD: The term of CVD designates any abnor

mality of the brain resulting from various pa
thological process of the blood vessels.

•Stroke is a syndrome characterized by the acu

te onset of a neurologic deficit that reflects foc
al/diffused involvement of the CNS and is the
result of a disturbance in the cerebral circulati
on network.
 Classification of CVD
• According to the lasting time of neurologic deficit:
• TIA (<24h)
• stroke (>24h).
• According to the severity of neurologic deficit:
• minor stroke
• major stroke
• silent stroke
• According to the pathological features:
• ischemic stroke
• hemorrhagic stroke
Blood supply in brain
• internal carotid artery (ICA) S.
ophthalmic artery
post communicating artery
anterior choroidal artery
anterior cerebral artery (ACA)
middle cerebral artery (MCA)
• ICA S. supplies blood for eyes and the 3/5
anterior part of cerebral hemisphere, namel
y,frontal lobe, temporal lobe, parietal lob
e and basil ganglion.
• the circle of Willis
• vertebral-basilar artery S.

• VA is divided into

• anterior spinal artery

• posterior spinal artery

• medullary artery

• posterior inferior cerebellar artery

– BA has following branches including

• anterior inferior cerebellar artery

• branches of pons

• internal auditory artery

• superior cerebellar artery
 • Posterior cerebral artery (PCA) is the termin
al division of BA

• VBA S. supplies blood for brainstem, cerebellu

m, 2/5 posterior part of cerebral hemisphere
(occipital lobe & basil area of temporal lobe) , i
nferior occipital lobe and thalamus.
TIA-Concept
• TIA is brief, repeated, reversible episodes of focal
ischemic neurologic disturbance. The duration o
f which should be less than 24h (usually lasting a
bout several min to 1h).
• Repeated TIAs of uniform type are more often a
warning sign of ischemic stroke.
TIA-Clinical findings

• Age of onset, 50~70, male > female

• Basic features:
• Transient episode (<24h)
• Reversible
• resolve completely
• repeated and uniform type
Clinical features of carotid artery TIA

• Common symptom/sign:
– weakness of opposite limbs.
• Characteristic symptom/sign:
– ophthalmic artery crossing paralysis
– Horner’s crossing paralysis
– Aphasia (dominant hemisphere is involved)
 Clinical features of carotid artery TIA
• Possible symptoms:
• contralateral single limb- or hemi-sensory deficit
• contralateral homonymous hemianopia
 TIA of Vertebra-basilar artery

• Common symptoms/signs:
– vertigo, dysequilibrium, usually no tinnitus
• Characteristic symptoms/signs:
– drop attack
– transient global amnesia （ TGA ）
– bioccular vision disorder
 TIA of Vertebral-basilar artery

• Possible symptoms/signs:
– swallowing disorder, dysarthria/dysphagia
– incoordination （ ataxia ）
– disturbence of consciousness with /without small pupil
s
TIA of Vertebral-basilar artery

• Possible symptoms/signs:
• unilateral/bilateral facial/perioral numbness or crossi
ng sensory deficit
• extraocular palsy or diplopia

• crossed paralysis
 TIA-treatment and prevention
• Treatment in terms of etiology
• Drugs for prevention
• Antiplatelet agents: Aspirin (ASA), Clopido
grel , Ticlopidine, Dipyridamole,
• Anticoagulation therapy: heparin, lower
molecule heparin, warfarin, Apixaban
TIA-treatment and prevention
• Drugs for prevention
• Others: Chinese traditional medicines, vasodilatation ag
ents, blood volume enlargement doses and surgical treat
ment （ carotid endoarterectomy, intralumenal stents ）
• Cerebral protective agents
cerebral infarction

• Concept: Cerebral infarction (CI) is necrosis and m

alacia of brain tissues due to ischemia and anoxi
a of the brain , which is in turn caused by deprive
d or insufficient blood supply in brain.
cerebral infarction

• Common types

cerebral thrombosis(CT)

cerebral embolism

cerebral watershed infarction

lacunar infarct
Pathophysiology
• Blood flow blockage >30 seconds--metabolic chan
ge, >1 min -- cease of neuron activity, >5min -- cer
ebral infarct.

• Ischemic penumbra

• time window (4.5h)

Clinical features
• Clinical types
• Complete stroke: reaches peak within several hours (<
6h)
• progressive stroke: reaches peak within 48h
• reversible ischemic neurological deficit (RIND): Lasting
>24h and recovering within 3ws
 Laboratory findings

• CT scan ： normal at the day of onset of the strok

e, shows the low density of the infarct after 24~48
h

• CT is preferred for initial diagnosis since it can ma

ke the critical distinction between ischemia and h
emorrhage
Laboratory findings

• MRI ： superior to CT scan in demonstrating early isc

hemic infarcts, showing ischemic stroke in brainstem
or cerebellum and detecting thrombosis occlusion of
venous sinuses.
Laboratory findings
• Cerebral angiography ： MRA, CTA, DSA
• Blood tests and ECG: Serum glucose, cholesterol and
lipid, hemorheology.
• TCD
• CTP
 Diagnosis and differentiation

• Diagnosis
• Prompt diagnosis of stroke should be ma
de through analysis of clinical features
(Patients presenting with focal central n
ervous system dysfunction of sudden ons
et, lasting more than 24hs)
• CT and MRI changes
• FAST (face, arm, speech, time)
Treatment in Acute Phase
• Thrombolysis: recombinant tissue plasminogen ac
tivator(rTPA, within 4.5h after onset)
• Endovascular treatment: arterial thrombectomy,
arterial thrombolysis (within 6h after onset)
• Bridging therapy
• Complications: Hemorrhage, reperfusion d
amage, brain edema, reocclusion
Treatment
• Two very important concepts
• Ischemic penumbra
• Time window
 Treatment
• Antiplatelet agents
• The regime is as described in the section of TIA.
• Anticoagulation agents: to prevent the progressio
n of thrombosis. The agents used are the same as
mentioned in the section of TIA.
• Statins: Lipitor, Rosuvastatin, etc.
• Blood pressure control
• Glucose control
• Fibrinogen degradation therapy: Defibrase, Batro
xobin, Ancrod, etc.
 Treatment
• Neuroprotective agents:
• Anti-free radical agents ： Ederavone, etc.
• CCBs ： Nimodipine, etc.
• Mild hyperthermia

• Rehabilitation treatment
Cardiology: hypertension
Aims

• When to initiate drug treatment?

• How low should BP be lowered?

• How do you get there?

Introduction

There are two types of hypertension:

• Primary: High blood pressure that is not related to anoth
er medical condition
• Secondary: Another medical condition that causes high bl
ood pressure, usually occurring in the kidneys, arteries, h
eart, or endocrine system. Examples include:
• Sleep problems like sleep apnea
• Blocked renal arteries in the kidneys
• Unusual levels of hormones controlling blood pressure
Diagnosis Definition

Category Systolic Diastolic

Optimal <120 and <80

Normal 120–129 and/or 80–84

High normal 130–139 and/or 85–89

Grade 1 hypertension 140–159 and/or 90–99

Grade 2 hypertension 160–179 and/or 100–109

Grade 3 hypertension ≥180 and/or ≥110

Isolated systolic hypertension ≥140 and <90

Diagnosis Accurate
Diagnosis Screening Causes

Causes of Secondary Hypertension

Common causes
Renal parenchymal disease
Renovascular disease
Primary aldosteronism
Obstructive sleep apnea
Drug or alcohol induced
Uncommon causes
Pheochromocytoma/paraganglioma
Cushing’s syndrome
Hypothyroidism
Hyperthyroidism
Aortic coarctation (undiagnosed or repaired)
Primary hyperparathyroidism
Congenital adrenal hyperplasia
Mineralocorticoid excess syndromes other than primary aldosteronism
Acromegaly
Diagnosis Stratification - old

Blood pressure (mmHg)

Other risk factors,
asymptomatic organ High normal SBP Grade 1 HT Grade 2 HT Grade 3 HT
damage or disease 130−139 SBP 140−159 or SBP 160−179 SBP ≥180
or DBP 85−89 DBP 90−99 or DBP 100−109 or DBP ≥110

No other RF Low risk Moderate risk High risk

Moderate to
1−2 RF Low risk Moderate risk High risk
high risk

Low to Moderate to
≥3 RF High risk High risk
moderate risk high risk

Moderate to High to
OD, CKD stage 3 or diabetes High risk High risk
high risk very high risk

Symptomatic CVD, CKD stage

Very high risk Very high risk Very high risk Very high risk
≥4 or diabetes with OD/RFs

Stratification of total CV risk in categories of low, moderate, high and very high risk according to SBP and DBP and prevalence of RFs,
asymptomatic OD, diabetes, CKD stage or symptomatic CVD. Subjects with a high normal office but a raised out-of-office BP (masked
hypertension) have a CV risk in the hypertension range. Subjects with a high office BP but normal out-of-office BP (white-coat hypertension),
particularly if there is no diabetes, OD, CVD or CKD, have lower risk than sustained hypertension for the same office BP.
BP, blood pressure; CKD, chronic kidney disease; CV, cardiovascular; CVD, cardiovascular disease; DBP, diastolic blood pressure;
HT, hypertension; OD, organ damage; RF, risk factor; SBP, systolic blood pressure.
Diagnosis Stratification - new
People with any of the following: Documented CVD, either clinical or
unequivocal on imaging.
• Clinical CVD includes acute myocardial infarction, acute coronary syndrome,
coronary or other arterial revascularization, stroke, TIA, aortic aneurysm and PAD.
• Unequivocal documented CVD on imaging includes significant plaque (i.e. >
Very high 50% stenosis) on angiography or ultrasound. It does not include increase in carotid
risk intima-media thickness.
• Diabetes mellitus with target organ damage, e.g. proteinuria or a with a major
risk factor such as grade 3 hypertension or hypercholesterolaemia
• Severe CKD (eGFR < 30 mL/min/1.73 m2)
• A calculated 10-year SCORE of > 10%
People with any of the following:
• Marked elevation of a single risk factor, particularly cholesterol > 8 mmol/L (>
310 mg/dL) e.g. familial hypercholesterolaemia, grade 3 hypertension (BP >
180/110 mmHg)
High risk • Most other people with diabetes mellitus (except some young people with type 1
diabetes mellitus and without major risk factors, that may be moderate risk)
• Hypertensive LVH
• Moderate CKD (eGFR 30-59 mL/min/1.73 m2)
• A calculated 10-year SCORE of 5-10%
People with:
Moderate • A calculated 10-year SCORE of 1% to < 5%
risk • Grade 2 hypertension
• Many middle-aged people belong to this category

People with:
Low risk • A calculated 10-year SCORE of < 1%
Management Lifestyle Changes
 Management Drugs
Contraindications
Drug
Compelling Possible
Diuretics (thiazides/thiazide- • Gout •Metabolic syndrome
type, e.g. chlorthalidone and •Glucose intolerance
indapamide) •Pregnancy
•Hypercalcemia
•Hypokalemia

Beta-blockers •Asthma •Metabolic syndrome

•Any high-grade sino-atrial or atrioventricular •Glucose intolerance
block •Athletes and physically active
•Bradycardia (heart rate < 60 beats per min) patients

Calcium antagonists   •Tachyarrhythmia

(dihydropyridines) •Heart failure (HFrEF, class III or
IV)
•Pre-existing severe leg oedema

Calcium antagonists •Any high-grade sino-atrial or AV block • Constipation

(verapamil, diltiazem) •Severe LV dysfunction (LV EF < 40%)
•Bradycardia (heart rate < 60 beats per min)

ACE inhibitors •Pregnancy • Women of child-bearing

angiotensin-converting •Previous angioneurotic oedema potential without reliable
enzyme •Hyperkalemia (potassium > 5.5 mmol/L) contraception
•Bilateral renal artery stenosis Cough

ARBs •Pregnancy • Women of child-bearing

Angiotensin II Receptor •Hyperkalemia (potassium > 5.5 mmol/L) potential without reliable
Blockers •Bilateral renal
2018artery
ESC/ESH guidelines
stenosis contraception
 Management Drugs

When to Allow BP to increase

•Diastolic BP < 70 or systolic BP < 120 and age 60 or older with one of the
following:
•Chest pain
•Rising creatinine
•Orthostatic symptoms
•Easy fatigability
•TIA like symptoms
•Or patient states, “I just don’t feel good.”
•60 years or older and diastolic BP < 60 or systolic BP < 110 even without
symptoms
•Allow permissive hypertension (systolic up to 160) if 70 years or older (even
if diabetic or albuminuria is present) with one of the following :
•Rising creatinine in CKD 3b or higher (GFR 44 or lower)
•Carotid artery disease with symptoms
•Diastolic BP < 70
 Question
A 58 year old African-American woman with diabetes and dyslipidemia has a BP of 158/94 confirmed on several office visits. Other than obesity, the exam is normal. Labs show normal renal function, well-controlled lipids on atorvastatin and well-controlled diabetes on m
etformin. Urine micro-albumin is mildly elevated.
•What is the drug of choice to start?
A.Hydrochlorothiazide D
B.Norvasc CCB
C.Lisinopril ACEI
D.Losartan ARB
E.Bystolic B
F.Combination therapy
Cardiology: heart failure
Introduction
Definition

•AHA/ACC 2013
• Heart failure is a complex clinical syndrome that results from
any structural or functional impairment of ventricular filling or
ejection of blood.
•ESC 2012
• Heart failure can be defined as an abnormality of cardiac structure or
function leading to failure of the heart to deliver oxygen at a rate
commensurate with the requirements of the metabolizing tissues,
despite normal filling pressures

•There is no single diagnostic test for heart failure because it is

largely a clinical diagnosis based on a careful history and physical
examination.
Introduction
Mechanism
Introduction
Mechanism
Introduction
Mechanism
Introduction
Terms

Related to EF: HFrEF (reduced ejection fraction: EF<40%)

HFmEF (mildly impaired EF: EF 40-49%
HFpEF (preserved ejection fraction: EF ≥50%)
Related to time-course: New onset, transient, chronic
Related to progression: Acute, stable, worsening
Related to location: Left heart, right heart, combined
Abolished: Diastolic HF, Congestive HF
Introduction
Etiology
VALVULAR HEART DISEASE MYOCARDIAL DISEASE
• Coronary artery disease
• Mitral
• Hypertension
• Aortic
• Cardiomyopathy
• Trisuspid
• Pulmonary
ENDOCARDIAL DISEASE
PERICARDIAL DISEASE • With/without hypereosinophilia
• Constrictive pericarditis • Endocardial fibroelastosis
• Pericardial effusion
HEART
ARRHYTHMIA
HIGH OUTPUT STATES FAILURE • Tachyarrhythmia
• Anaemia • Atrial
• Sepsis • Ventricular
• Thyrotoxicosis • Bradyarrhythmia
• Paget‘s disease • Sinus node dysfunction
• Arteriovenous fistula CONDUCTION DISORDERS
• Atrioventricular block
VOLUME OVERLOAD
• Renal failure
• Iatrogenic (e.g. post-operative
CONGENITAL
fluid infusion HEART DISEASE McMurray et al. Eur Heart J 2012;33:1787–847
Diagnosis Symptoms

The diagnosis of HF can be difficult, especially in the early stages

Symptoms Signs
Typical More specific
Breathlessness Elevated jugular venous pressure
Orthopnoea Hepatojugular reflux
Paroxysmal nocturnal dyspnoea Third heart sound (gallop rhythm)
Reduced exercise tolerance Laterally displaced apical impulse
Fatigue, tiredness, increased time to Cardiac murmur
recover after exercise
Ankle swelling
 Diagnosis Stages
ACC/AHA stages of HF
(based on structure and damage to heart)
Stage A At high risk for HF, but without
structural or functional
abnormality
No signs or symptoms
Stage B Developed structural heart
disease strongly associated with
development of HF, but without
signs or symptoms
Stage C Symptomatic HF associated with
underlying structural heart
disease
Stage D Advanced structural heart Class IV
disease and marked symptoms of
HF at rest, despite maximal
medical therapy
NYHA functional classification
(based on symptoms or physical activity)
Class I No limitation of physical activity.
Ordinary physical activity does not
cause undue fatigue, palpitation or
dyspnoea
Class II Slight limitation of physical activity.
Comfortable at rest, but ordinary
physical activity results in HF
symptoms
Class III Marked limitation of physical
activity. Comfortable at rest, but
less than ordinary activity results in
HF symptoms
Symptoms of HF present at rest. If
any physical activity is undertaken,
discomfort is increased
Diagnosis Stages

HF is a silently progressing disease

We begin to look at the disorder at the end of its natural history - that is too late!

Vascular Remodeling
environmental
determinants

LVH
Diastolic Diastolic Heart
CVD risk Dysfunction Failure
physical Disturbed
factors &
activity ↓ Microcirculation
biomarkers Systolic Systolic
Dysfunction Heart Failure
CAD / Infarktion
genetic
determinants
Myocardial Remodeling

Stage A B C/D
Diagnosis Stages

The diagnosis of HFpEF is more difficult than the diagnosis of HFrEF

The diagnosis of HFrEF requires three conditions to be satisfied
1. Symptoms typical of HF
2. Signs typical of HF
3. Reduced LVEF

The diagnosis of HFpEF requires four conditions to be satisfied

1. Symptoms typical of HF
2. Signs typical of HF
3. Normal or only mildly reduced LVEF and LV not dilated
4. Relevant structural heart disease (LV hypertrophy/LA
enlargement) and/or diastolic dysfunction

HFpEF: HF despite absence of pump failure

Half of patients with HF have HFpEF
Diagnosis BNP

ESC HF diagnostic algorithm 2012

Acute onset Non-acute
onset
ECG, Chest x-ray ECG, Possibly chest x-ray

Echocardiography BNP/NT-pro BNP* BNP/NT-pro BNP Echocardiography

ECG normal and ECG abnormal or ECG abnormal or ECG normal and
NT-proBNP < NT-proBNP > NT-proBNP > 125 NT-proBNP <
300pg/mL or 300pg/mLb or pg/mLa or 125pg/mL or
BNP < 100 pg/mL BNP > 100 pg/mL b BNP > 35 pg/mL a BNP < 35 pg/mL

HF unlikely c
HF unlikely c
Echocardiography

If heart failure is confirmed by

echocardiography, determine aetiology and
start appropriate treatment.
 Diagnosis BNP

HFA/ESC diagnostic recommendations HFpEF

Symptoms or signs of HF

Normal or mildly reduced LV systolic function (LVEF >50% and LVEDVI <97 mL/m 2)

Evidence of abnormal LV relaxation, filling, diastolic distensibility, and diastolic stiffness

Invasive hemodynamic TD Biomarkers

measurements EIE′ >15 15 >EIE′ >8 NT-proBNP >220 pg/mL or
mPCW >12 mmHg BNP >200 pg/mL
or LVEDP >16 mmHg
or  >48 ms
or b >0.27
Biomarkers Echo – blood flow Doppler TD
NT-proBNP EIA>50 yr <0.5 and DT>50 yr >280 ms EIE′ >8
>220 pg/mL or or Ard–Ad >30 ms
BNP >200 pg/mL or LAVI >40 mL/m2
or LVMI >122 g/m2(♀); >149 g/m2 (♂)
or atrial fibrillation

E = early mitral valve flow

velocity; Eʹ= early TD lengthening HFpEF
velocity
Diagnosis BNP

Particular relevance of BNP

• diagnosis
• staging
• risk stratification
• monitor/titrate therapy
• admission/discharge decisions:
> rule out symptomatic LV dysfunction

A normal natriuretic peptide level in an untreated patient virtually excludes

significant cardiac disease
Consider different cut-off values in various clinical situations
 Treatment From risk factors

Objectives of treatment for chronic HF

1. Prognosis • reduce mortality
2. Morbidity • relieve symptoms and signs
• improve QoL
• eliminate edema and fluid retention
• increase exercise capacity
• reduce fatigue and breathlessness
• reduce the need for hospitalization
• provide end of life care
3. Prevention • occurrence of myocardial damage
• progression of myocardial damage
• remodelling of the myocardium
• reoccurrence of symptoms and fluid accumulation
• hospitalization
Treatment Therapeutic Targets

Protect/Preserve myocardium Improve hemodynamics

• RAAS inhibitors • Digoxin
• -blockers • Diuretics
• Hydralazine/Nitrates

Prevent ischemic events Prevent sudden arrhythmic

• Revascularization death
• Antiplatelet agents • -blockers
• Statins • Implantable cardioverter-
defibrillator
 Treatment HFpEF vs. HFrEF

Potential Therapeutic
Targets
Treatment HFpEF HFrEF
• Preload Diuretics YES YES
• Afterload CCBs YES NO
• Contractility Beta-blockers NO YES

• Remodeling ACEIs NO YES

ARBs NO YES
MR antagonists NO YES
Ivabradine NO YES
Digoxin NO YES
H-ISDN- Isosorbide dinitrate NO YES
ARNIs PARAGON-HF study YES
Question

Which of the following statements about natriuretic

peptides is NOT correct?
A. Circulating levels of both atrial natriuretic peptide and brain
natriuretic peptide (BNP) are elevated in patients with heart failure
B. Plasma BNP level is useful in distinguishing cardiac from noncardiac
causes of dyspnea in the emergency department setting
C. Elevated plasma BNP levels predict adverse outcomes in patients with
acute coronary syndromes
D. Prohormone BNP is cleaved into the biologically inactive N-terminal
(NT) proBNP and biologically active BNP
E. Circulating levels of NT-proBNP levels decrease with age
Cardiology: coronary heart disease
Introduction
Risk Factors
 Age
 Gender - female (<50 years, before menopause)

 Elevated serum lipids

 Hypertension
 Tobacco use
 Physical inactivity
 Obesity
 Diabetes
 Metabolic syndrome
 Psychologic states (Dual-heart disease)
Introduction
From Subclinical Atherosclerosis to Plaque Progression and Acute Coronary Events
Introduction
From Subclinical Atherosclerosis to Plaque Progression and Acute Coronary Events

1) foam cell to
2) extracellular lipid in the
subintima to
3) fibrofatty stage to
4) procoagulant expression
and weakening of the
fibrous cap.
5) ACS develops with
disruption of the fibrous
cap, which is the stimulus
for thrombogenesis.
6) Thrombus resorption
may be followed by
collagen accumulation
and smooth muscle cell
growth.
Diagnosis Category of CAD
Diagnosis
Diagnosis Chest pain

Chest pain

Cardiac Non - Cardiac

Non-CAD CAD Urgent Non-urgent

Non-urgent Urgent Urgent Non-urgent

Stable

Unstable angina
STEMI
NSTEMI
Diagnosis Chest pain
Diagnosis Stable angina
Diagnosis ECG

J point in a) normal; b) c) J point elevation; d) J

point depression; e) with J wave (Osborn wave)
 Diagnosis ECG

• ST-segment
1. Changes in QRS complex, ST segment, and T wave
2. Distinguish between STEMI and NSTEMI
3. Pathologic Q wave (QRS)
4. To judge the infarcted location (wall and culprit artery)
 Diagnosis ECG

• ST-segment elevation

Definition of STEMI
– New ST elevation at the J point in two
contiguous leads of > 0.1mV in all leads
other than leads V2-V3

– For leads V2-V3 the following cut

points apply: ≥0.2 mV in men ≥40
years, ≥0.25 mV in men <40 years, or
≥0.15 mV in women

Other special signs

• new left bundle branch block (LBBB)
• pathological Q waves
 Diagnosis ECG

• ST-segment elevation

Other causes
Myocarditis
Pericarditis
Benign early repolarizatio
n
Left bundle branch block
Left ventricular hypertrophy
Ventricular aneurysm
Brugada syndrome
Ventricular paced rhythm
Acute Pericarditis causes
widespread concave
(“saddleback”) ST segment
elevation with 
PR segment depression in
multiple leads, typically involving
I, II, III, aVF, aVL, and V2-6.
 Diagnosis ECG
• ST-segment ↑
1. To judge the infarcted location (wall and culprit artery)
•Septal (V1-2)
•Anterior (V3-4)
•Lateral (I + aVL, V5-6)
•Inferior (II, III, aVF)
•Right ventricular (V1, V4R)
•Posterior (V7-9)
Inferior……………………………………RCA, LCx
Inferior RV……………………………..Proximal RCA
Inferoposterior……………………….RCA, LCx
Isolated RV…………………………….LCx
Isolated Posterior………………….RCA, LCx
Anterior………………………………….LAD
Anteroseptal…………………………..LAD
Anteroseptal-lateral……………….Proximal LAD
Anterolateral, inferolateral, or
Posterolateral…………………………LCx
Diagnosis ECG-evolution
 Diagnosis ECG

• ST Segment depression-NSTE-ACS
 Diagnosis ECG

• STE-ACS VS NSTE-ACS
 Diagnosis Differential diagnosis

• Unstable angina VS MI
Diagnosis Agorithm
Diagnosis Diagnostic gap
Diagnosis Coronary Angiography
Diagnosis Coronary Angiography

TMP Grade 3 TMP Grade 2 TMP Grade 1 TMP Grade 0

Normal ground glass Dye strongly persistent Stain present No or minimal blush
appearance of blush at end of washout Blush persists
Dye mildly persistent Gone by next injection on next injection
at end of washout
Normal Slow Stain Pale

TIMI Myocardial Perfusion (TMP) Grades

Gibson et al, Circulation 2000

Diagnosis Types
Treatment

Methods
• Life style change
• Drugs
• PCI and CABG
Treatment Stable angina

Drugs of Stable Angina

Treatment Angina Improved Prognosis
control Prevention of MI
Nitrates Yes No
 Blockers Yes Yes
Ca++ blockers
Dihydropyridines: short acting Poor No (prognosis )
: long acting Yes ?
Diltiazem, Verapamil Yes ? No
Aspirin No Yes
Statin ?Yes Yes
ACEI ?Yes Yes
PTCA Yes ?
CABG Yes Yes
Treatment Stable angina

Consideration of Revascularization Therapy

• the greater the number of vessels involved.
• there is left main stem stenosis of >50%.
• the proximal LAD is involved.

• PCI reduces the incidence of angina

• No study has demonstrated that PCI improves survival rates in Stable
angina
• PCI may increase the short-term risk of MI
• PCI does not lower the long-term risk of MI
Treatment Stable angina

Consideration of Revascularization Therapy

• the greater the number of vessels involved.
• there is left main stem stenosis of >50%.
• the proximal LAD is involved.
Recommendation Strength of Level of
recommendation evidence
We recommend that coronary angiography be Strong High
considered early in patients who are identified to have quality
high risk non-invasive test features

We recommend that patients who develop medically Strong High

refractory symptoms or inadequate CV quality of life quality
on medical therapy should undergo elective coronary
angiography in anticipation of possible
revascularization procedures
Treatment ACS The best choice - PCI

 Pharmacologic Fibrinolysis (STEMI ONLY)

 Percutaneous coronary intervention
 Possible surgical measures (CABG)
Treatment ACS The best choice - PCI
Treatment ACS Antiplatelet
Treatment ACS Antiplatelet

COR LOE Recommendations

In patients with ACS (NSTE-ACS or STEMI) treated with
DAPT after BMS or DES implantation, P2Y12 inhibitor
I B-R therapy (clopidogrel, prasugrel, or ticagrelor) should be
given for at least 12 months.

In patients treated with DAPT, the recommended daily

I B-NR dose of aspirin is 81 mg (range, 75 mg to 100 mg).
Treatment ACS beta-blocker

Class I
Oral beta-blocker therapy should be initiated within the
first 24 hours in patients who do not have any of the
following: 1) signs of HF, 2) evidence of low-output state,
3) increased risk for cardiogenic shock, or 4) other
contraindications to beta blockade (eg, PR interval >0.24
second, second- or thirddegree heart block without a
cardiac pacemaker, active asthma, or reactive airway
disease).240–242
(Level of Evidence: A)
Question

It is very important to distinguish whether the p

atient is having an ST-elevation MI (STEMI) or a
non–STEMI (NSTEMI)

Why?
Happy graduation and wish you a
bright future.
Tao Zhan, MD
The First Hospital of Changsha