Acute Coronary Syndrome (ACS)

a set of signs and symptoms related to decreased blood flow to the heart. ACS is compatible with a diagnosis of acute myocardial ischemia, but it is not pathonomonic.

Manifestations

• chest pain
• tightness around the chest and radiating to the left arm and the left angle of the jaw.
• may be associated with diaphoresis
• nausea
• vomiting
• shortness of breath.
•  Some may report palpitations
• feeling of anxiety
• sense of impending doom

Diagnosis of MI:

• ECG
• Blood tests – troponin marker levels

Mycobacterium Tuberculosis (TB)

 

Tuberculosis

Etiology

• Caused by M. tuberculosis

• can infect any organ of the body, yet most often the lungs
• Strains specific to human infection

1. M. tuberculosis hominis
2. M. tuberculosis bovis
3. M. avium intracellular (this strain infects only immunocompromised persons)

 

Modes of Transmission

• airborne transmission – respiratory secretions

1. coughing
2. sneezing
3. talking

• consumption of contaminated dairy products – M. tuberculosis bovis

 

TB and HIV infection association

• antibiotics in the 1950’s decreased TB infection rates in western countries
• Rise of HIV in the 1980’s resulted in increased infection rates
• Largest caseload of TB infections occurred between 1985-1993
• after 1993 infection rates again declined with increased resources to screening, prevention and support for AIDS patients.
• TB continues to be prevalent in developing countries with high HIV rates
• antibiotic resistant strains have now emerged

 

Pathophysiology

Cell-mediated immune response results in tissue hypersensitivity and resistance to TB antigens.

Hypersensitivity immune response to the infection results in the destructive aspects of the disease.

1. Cavitation
2. Caseating necrosis

 

Macrophages: the primary cell infected by the bacterium.

Mode of infection:

1. infected airborne droplets pass down bronchial tree
2. settle in alveoli
3. alveolar macrophages phagocytize, yet do not kill
4. macrophages initiate the cell-mediated immune response
5. TB has no surface antigens to promote early immunoglobulin response

 

Primary TB

• Develops in previously unexposed individuals
• most develop latent infection – non-active, non-transmitable, infection walled off in granulomas
• progressive primary TB develops in 5% of cases
• results in lung tissue destruction and spread to multiple sites
• immunocompromised individuals are likely to develop progressive primary TB

 

Ghon’s complex: granulomatous lesion where infection has been walled off by the immune system.

Secondary TB. Discuss the pathophysiology of each form of the disease.

Mention how secondary infection might occur.

• Indicative of reinfection from inhaled droplets or reactivation of previously healed primary lesions
• occurs in cases of impaired immune defenses
• partial immunity that follows primary TB affords some protection against reinfection
• cell-mediated hypersensitivity can be an aggravating factor (cavitation and bronchial dissemination)
• pleural effusion and tuberculosis empyema are common progressions

 

Manifestations

Primary TB:

1. fever
2. weight loss
3. fatigue
4. night sweats

 

infection onset may present with:

1. high fever
2. pleuritis
3. lymphadermitis

 

Secondary TB

1. low-grade fever
2. night sweats
3. fatigue, low endurance
4. anorexia
5. weight-loss
6. initial dry cough progressing to purulent and sanguinous sputum
7. Dyspnea (advanced)
8. Orthopnea (advanced)

 

Diagnostics

1. Tuberculose skin test

• indicates delayed hypersensitivity rxn (cell-mediated, type IV) following exposure
• a positive skin reaction is not indicative of active TB
• false-positives may result in cases of cross rxn with non-tuberculosis mycobacterium such as M. avium-intracelluar
• false-negatives may occurs in immunocompromised individuals where low or no immune response is mounted against the pathogen

1. Chest X-ray
2. Culture

• for definitive diagnosis of active TB

• individuals who test positive usually remain so for the remainder of their lives

 

Treatment and Management

• Multi-antibiotic regime to prevent further development of resistant strains
• chemotherapy is required for prolonged duration
• prophylactic treatment is used for infected individuals without active TB

1. those who have come in contact with active cases
2. those who have converted from negative to positive skin test within the last 2 years
3. those with a Hx of untreated or inadequately treated TB

 

Antibiotics:

1. INH
2. rifampin
3. pyrazinamide – PZA
4. ethambutol
5. streptomycin – first drug used to treat, now some strains are resistant

 

Immunization

1. Bacillus Calmette-Guerin (BCG) Vaccine

• used to prevent infection in those at high risk
• it is the only vaccine available

Medical Fun and Games

Like a flower waiting to bloom
Like a lightbulb in a dark room
I’m just sitting here waiting for you
To come home and turn me on

Like the desert waiting for the rain
Like a school kid waiting for the spring
I’m just sitting here waiting …

 - Norah Jones

Antiemetics

 

• treat nausea and vomiting
• act by inhibiting dopamine or serotonin receptors in the brain
• act to block various pathways preventing signals from reaching the VC or CTZ

 

Physiologic vomiting triggers

1. Stimulus of the vomiting center – VC
2. Stimulus of the chemoreceptor trigger zone – CTZ

 

Secondary to nausea and vomiting is dehydration

• excessive fluid loss can lead to acid-base disturbances

 

Types of antiemetics

1. anticholinergics
2. Antihistamines
3. Benzodiazepines
4. Cannabinoids
5. Glucocorticoids
6. Phenothiazines
7. Serotonin Receptor Antagonists

 

Acholinergics (Scopalamine)

• block Ach receptors in the vestibular nuclei and reticular formation
• prevent stimuli from these areas being transmitted to VC or Chemoreceptor trigger zone

 

Antihistamines (Gravol or dimenhydrinate)

• bind histamine receptors inhibiting the binding of Ach to vestibular nuclei and reticular formation

 

Neuroleptic agents (Phenothiazines)

• block dopamine receptors in the chemoreceptor trigger zone
• meds also relieve vertilago
• use in chemo tx of nausea and vomiting

 

Prokinetic agents (Maxeran)

• blocks dopamine in the CTZ and stimulates GI peristalsis
• acts to tighten gastroesophageal sphincter preventing GERD
• aids in gastric emptying – used for tube feed pts
• Maxeran must be reduced if diarrhea develops
• SE – drowsiness

 

Serotonin blockers (Odancetron aka Zofran)

• blocks serotonin receptors in the GI, VC and CTZ
• often effective when gravol is not

Benzodiazepines (Ativan)

• decreases response in VC and CTZ
• used as a adjunct to treat nausea and vomiting, not alone
• uncommon in the tx of nausea and vomiting

 

Glucocorticoids

• action in N and V tx unclear
• used in adjunct with other antiemetics
• used in chemo related N and V
• not a first line antiemetic due to it being a steroid, decreasing immunity and elevating the WBC count

 

Antiemetic considerations:

• liver and kidney Fx
• Fluid and electrolyte balance (dehydration risk)
• BP & P – hypovolemia risk

 

Antiemetic choice considerations

1. if vomiting occurs after a meal, administer prior to meal
2. If gravol is ineffective use Serotonin blockers (Odancetron)

Laryngitis

Inflammation of the larynx and surrounding mucous membranes.

Manifestations:

• Pain and Inflammation of the mucous membranes of the larynx,
• Loss of Voice – hoarseness
• coughing

Etiology:

• viral, bacterial or fungal infection
• physical trauma to the throat of neck or overuse of the vocal cords
• excessive coughing, smoking, or alcohol consumption

Treatment and Management

1. Treatment of pathogen by antifungal or, antibacterial agents
2.  Reduction of high-impact stress to the vocal cords caused by loud, frequent, and high-pitched voicing is recommended
3. If laryngitis is due to gastroesophageal reflux: The patient may be instructed to take a GERD treating agents for a period of 4-6 weeks.

Like starlight on snow…

The winter sky above us
Was shining
In moonlight,
And everywhere around us
The silence
Of midnight.
And we had gathered snowflakes;
Remember
The soft light
Of starlight on snow.

Oooh, remember this,
For no-one knows
The way love goes.
Oooh, remember this,
For no-one knows
The way life goes.

- Enya

Kawasaki’s disease (Mucocutaneous lymph node syndrome)

a multisystemic necrotizing medium vessel vasculitis

largely seen in children under 5 years of age

etiology:

autoimmune disease

pre-existing viral infection trigger

Manifestatations:

multi-organ affects

• erythmatous peidermis
• erythmatous muscous membranes
• cervial lymph node enlargement
• blood vessel walls
• heart – can cause severe aneurysmal dilations in untreated children
• edema in hands and feet
• fever may accompany other symptoms

Treatment:

• corticosteriods
• Immunogolgulin therapy
• NSAIDs – asprin

Macular degeneration

eye disease caused by degeneration of the cells of the macula lutea and results in blurred vision; can cause blindness

2 types:

1. wet
2. dry

• In the wet (exudative) form, which is more severe, blood vessels grow up from the choroid behind the retina.
• The retina can also become detached.
•  In the dry (nonexudative) form, cellular debris called drusen accumulate between the retina and the choroid.
• The retina can become detached.

Treatment:

laser coagulation

medication that stops and sometimes reverses the growth of blood vessels

Smallest of gifts

Somewhere
in a winter night
the angels
begin their flight;
dark skies
with miles to go,
no footsteps
to be lost in snow.

one is sorrow
one is peace
one will come
to give you sleep
one is comfort
one is grief
one will take
the tears you weep

New star
in a midnight sky
in heaven
all the angels fly
soft wings so true
and all things
they will give to you

Somewhere
in a winter night
the angels
begin their flight

Journey of angels – Enya

Rhinosinusitis

 

Inflammation of the nasal passages and sinusitis – paranasal inflammation.

Etiology

• a blockage at the ostia that drain the sinuses
• viral upper respiratory tract infections
• allergic rhinitis
• Nasal polyps (constant irritant)
• barotrauma due to changes in barometric pressure (damage)
• abuse of nasal decongestants

 

Pathophysiology of the affected sinuses

• The nasal cavities are continuous with the paranasal sinuses.
• Upper respiratory tract infections frequently precede or occur in conjunction with sinus infections.

 

Manifestations

1. facial pain
2. purulent nasal discharge
3. decreased sense of smell
4. fever
5. pain on bending
6. unilateral maxillary pain

 

Diagnosis

• Hx and Px of nose and throat
• headache must be differentiated from other causes
• differentiate between viral and bacterial rhinosinusitis
• viral rhinosinusitis resolves within 7 days
• bacterial rhinosinusitis may be present if symptoms worsen after 5-7 days or progress beyond 10 days
• Immunocompromised individuals may present with fever, rhinorrhea, or facial edema, yet other signs may be absent
• chronic rhinosinusitis may escalate to nasal obstruction, hoarseness and/or chronic cough

 

Treatment

• antibiotics for secondary bacterial infection
• mucolytic agents
• symptom relief
• 2/3rds of those with acute bacterial rhinosinusitis recover without antibiotics
• Surgery may be used to correct obstructed ostiomeatal openings

 

Complications

• due to sinus proximity to the brain and orbital wall, infections can lead to intracranial and orbital wall complications
• seen most commonly with frontal and ethmoid sinus infections
• Orbital complications can range from edema of the eyelids to orbital cellulitis and subperiosteal abscess formation