Heart Failure, Stroke , PE,DVT, Afib,MI And Emerging Diseases Flashcards

1
Q

What is heart failure

A

Clinical syndrome that develops when the heart cannot maintain adequate output, or can do so only at the expense of elevated ventricular filling pressure.

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2
Q

Which group of people commonly get HF and which year group is it prevalent

Prognosis is
•Poor if untreated true or false

A
•Common in the elderly
•Prevalence
•1% : 50 – 59
•10% : 80 – 89
•

True

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3
Q

What is the pathophysiology of heart failure which causes a viscous cycle in the progression of heart failure

A

When there is increased blood pressure and cardiac work there is myocyte loss and myocardial fibrosis
This causes heart failure due to reduced cardiac output
This leads to neurohormonal activation (sympathetic nervous system,RAAS,vasopressin,endothelin system) this causes vasoconstriction and increased afterload and thus causes increased bp and cardiac work or the neurohormonal activation causes sodium and water retention leading to increased intravascular volume and increased bp and cardiac work

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4
Q

Types of heart failure and explain em

A

Left Heart Failure
•Reduction in left ventricular output and an increase in left atrial and pulmonary venous pressure

Right Heart Failure
•Reduction in right atrial pressure and an increase in right atrial and systemic venous pressure

Biventricular
•Failure of the left and right heart may develop because of a disease process

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5
Q

Name the other types of heart failure and explain

A

Systolic Dysfunction
•Heart failure as a result of impaired myocardial contraction

  • Diastolic Dysfunction
  • Heart failure as a result of poor ventricular filling and high filling pressures as a result of abnormal ventricular relaxation
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6
Q

And name the other other types of heart failure and explain

A

Acute Heart Failure
•Heart failure that develops suddenly

  • Chronic Heart Failure
  • There is gradual impairment of cardiac function with several compensation
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7
Q

What factors precipitate or aggravate heart failure in pre existing heart disease

A

Myocardial ischemia or infarction
Intercurrent illness example-infection
Arrhythmia example-atrial fibrillation
Inappropriate reduction of therapy
Administration of a drug with negative inotropic (beta blockers) or fluid retaining properties (NSAIDS,corticosteroids)
Pulmonary embolism
IV fluid overload example post operative IV infusion
Conditions associated with increased metabolic demand example anemia,pregnancy,thyrotoxicosis

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8
Q

What are the four clinical features each of left and right heart failure
( failure to thrive and difficulty feeding in kids )

A
Left heart failure-
Pulmonary edema 
Raised JVP
Pleural effusions
Pitting edema 
Orthopnea 
Right-
raised JVP
Hepatomegaly 
Ascites which causes decreased preload and cardiac output 
Peripheral pitting edema
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9
Q

What are the differentials for peripheral edema

A

Cardiac failure -right or combined left and right heart failure,pericardial constriction,cardiomyopathy

Chronic venous insufficiency-varicose veins

Hypoalbuminaemia- nephrotic syndrome,liver disease,protein losing enteropathy ;often widespread,can affect arms and face

Drugs;
Sodium retention;fludrocortisone,NSAIDS
Increasing capillary permeability;nifedipine and amlodipine

Idiopathic;occurs in women more than men

Chronic lymphatic obstruction

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10
Q

What are the six investigations for heart failure

A

~~~
Chest X-ray
•ECG
FBC ( anemia can precipitate it)
Echocardiogram
•Serum Urea, Creatinine and Electrolytes
•Full Blood Count
•Thyroid Function Test ( thyrotoxicosis can precipitate it)
Lipid profile and cardiac enzymes( MI can precipitate it)
Fasting blood sugar

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11
Q

How is acute heart failure managed

A
Prop patient up – to relieve pulmonary congestion
•Give Oxygen
•High flow, high-concentration
•Non-invasive positive pressure ventilation
•CPAP: 5 – 10mmHg
•Give Loop Diuretics
•60 – 120mmHg IV Furosemide
•Give Nitrates
•IV Glyceryl trinitrate 10-200ug/min

The use of continuous positive airway pressure (CPAP) therapy has been reported to reduce the risk of death and hospitalization in heart failure patients with OSA (4). Moreover, CPAP use ameliorates the cardiac function through mainly decreasing afterload in heart failure patients with

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12
Q

What is the non pharmacological management of heart failure

A

Educate the person on the disease
Check the persons diet and weight reduction if person is obese
Avoid food with high salt content
Moderate or eliminate alcohol drinking but it should be eliminated in people with alcohol induced cardiomyopathy
Stop smoking
Regular exercise
Prop up in bed
Consider influenza and pneumococcal vaccination

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13
Q

Pharmacological management of Hf

A

If patient comes boom:
ABcs, oxygen, pain meds in there is pain then add the propping up in bed to relive pulmonary congestionthen add these drugs
1.* Diuretic Therapy IV furosemide and
2. Angiotensin-converting enzyme inhibition therapy or Angiotensin Receptor Blocker if ACEi isn’t tolerated
3. Beta-adrenoceptor blocker therapy
Identify and treat precipirating causes ( hpt, infections, anemia, MI, thyrotoxicosis)
Refer when patient is stable ( if in health center so that specialist will identify and treat underlying cause )

Give Digoxin if there’s an AFib
* Used in heart failure and atrial fibrillation
* Vasodilators such as dobutamine given when there’s hypotensionfue to cardiogenic shocks
Give enoxaparin for prophylactic anticoagulant against venous thrombosis

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14
Q

What other devices were used in HF
State the NYHA class of heart failure

A

Impaired Cardiac defibrillators and resynchronisation therapy
•Coronary revascularisation
•Heart transplantation
•Ventricular assist devices

NYHA class
Class 1- no symptoms or no limitations when performing physical activities or can perform any physical activity without any symptoms
Class II- mild limitation when performing physical activities . Ordinary physical activity results in symptoms and is relived by resting
So for class two, heavy activities will cause the symptoms
Class III- marked limitation of physical activity. symptoms when performing slight physical activities and comfortable by resting but for stage 3 even bathing yourself or any small thing you do will cause the symptoms to come( fatigue palpitations and dyspnea )
Class IV- symptoms even at rest and cannot perform any physical activities at all without discomfort

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15
Q

Name five complications of Hf

A
Renal failure
•Hypokalaemia
•Potassium losing diuretics, hyperaldosteronism from RAAS activation
•Hyperkalaemia
•ACE-Is
•Hyponatraemia
•Feature of severe heart failure
•Poor prognosis
Complications
•Impaired liver function
•Liver congestion
•Thromboembolism
•Low cardiac output and impaired mobility
•Atrial and ventricular arrhythmias
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16
Q

What’s re the signs of right and left ventricular heart failure? CCF should be distinguished from which disease? Using which signs?(name additional signs of CCF and signs of the other disease)

A

HEART FAILURE
The signs of right ventricular heart failure are:
1. Raised pulsatile jugular venous pressure.
2. Hepatomegaly which is soft and tender.
3. Sacral and ankle oedema.

The signs of left ventricular failure are:

  1. Cardiomegaly; apex best is displaced outwards and downwards.
  2. Bilateral basal crackles which persist after coughing.

If a patient’s symptoms and signs suggest the presence of heart failure it is important to remember that this is a description and not a full diagnosis. Congestive cardiac failure (right heart failure secondary to left heart failure) must be distinguished from cor-pulmonale (right heart failure, secondary to lung disease).
Additional signs in congestive heart failure are basal lung crackles due to pulmonary oedema and pink frothy sputum as well as symptoms and signs suggesting left ventricular disease.
Additional signs of cor-pulmonale are coarse lung crackles as in bronchiestasis or fibrosing alveolitis, sputum which is sticky, white, grey, yellow or green.
There may also be symptoms and signs of chronic lung disease as well as right ventricular hypertrophy.

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17
Q

What are the typical patients of CCF,major signs and symptoms,investigations

A

Typical patient
 Patient with acute myocardial infarction or known left ventricular disease

Major symptoms
 Severe dyspnoea and variable circulatory collapse

Major signs
 Low-output state (hypotension, oliguria, cold periphery); tachycardia; S3; sweating; crackles at lung bases
Diagnosis
 CXR: bilateral air space consolidation with typical perihilar distribution
 Echocardiogram: usually confirms left ventricular disease
Additional investigations
 ECG: may show evidence of acute or previous myocardial infarction
 Blood gas analysis: shows variable hypoxaemia
Comments
 Although most cases are caused by acute myocardial infarction or advanced left ventricular disease, it is vital to exclude valvular disease or myxoma, which are potentially correctable by surgery

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18
Q

What are emerging diseases

A

Emerging infectious diseases are infections that have recently appeared within a population or those whose incidence or geographical range is rapidly increasing or threatens to increase in the near future

In other words, emerging diseases are diseases of infectious origin whose incidence in human has increased within the past decades or threatens to increase in the near future.

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19
Q

State three reasons for emerging diseases

A

Causes
Emerging diseases can be caused by;
●Previously untreated or unknown infectious agents
●Known agents that have spread to new geographic locations or new populations
●Re-emergence of agents whose incidence of disease had significantly declined in the past, but whose incidence of disease has reappeared. These are usually known as re-emerging diseases.

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20
Q

State five ways emerging diseases are transmitted

A
oPersonal contact
oAir droplet
oWater
oFomites (tables, door knobs, etc)
oZoonosis
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21
Q

State three groups of risk factors that can cause an emerging disease and give examples under each

A

A•Agents:
•Evolution of pathogen over time
•Resistance by pathogens to medications

c. Environment
•Climate change

b. Host
•War
•Poverty
•International travels
•Population growth
•Ural-urban migration
•Misuse of resources
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22
Q

What is the criteria for classifying a diseases condition as an emerging disease

A

For an emerging disease to become established, at least two (2) events have to occur;
•The infectious agent has to be introduced into a vulnerable population
•The agent has to have the ability to spread readily from person-to-person and cause disease. The infection also has to be able to sustain itself within the population; that is more and more people continue to be infected.

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23
Q

State six examples of emerging diseases

A
SARS (Severe Acute Respiratory Syndrome)
•MERS-CoV (Middle East Respiratory Syndrome Coronavirus)
•Influenza
•Ebola
•Rift Valley fever
•Escherichia coli 0157:H7 (E. coli)
•Dengue
•Tuberculosis
•Zika
•COVID-19
•Nipah and henipaviral diseases
•HIV/AIDS
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24
Q

What is influenza
What is it common for known as?
What causes it?
The RNA that causes it is highly variable.It is relatively unstable at room temperature. What is it’s half life ?
Why is there a species barrier with this RNA?

A

Influenza, commonly known as the “the flu” is an illness caused by RNA viruses (has an RNA genome of 8 genes) of the family Orthomyxoviridae; the influenza virus that infect the respiratory tract of many humans.

A few hours

Because of the structure of HA protein or hemagglutinin

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25
Q

. In the 2009 flu pandemic, the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses what are those viruses?––

the new strain appears to be as a result of what?

A

North American swine influenza, North American avian influenza, human influenza and swine influenza virus typically found in Asia and Europe

reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1.

26
Q

What is the pathophysiology of influenza

State the types of influenza viruses

A

influenza virus is an 8 segments of single-stranded RNA enclosed in a protein called capsid. The capsid is surrounded by a lipoprotein envelope that it gains from the host during maturation. The lipoprotein envelope has glycoprotein spikes all over it. These glycoproteins are neuraminidase (N) and hemagglutinin (H).
The hemagglutinin allows the virus to recognize and attach to receptors on the host epithelial cells and enters via endocytosis. Viruses with these hemagglutinin cause the red blood cells to agglutinate. This can be used to determine the presence of the virus.
Neuraminidase is an enzyme that helps the release of virions from the host cell.
Influenza viruses bud out of the host cell taking along some of the host lipoproteins with it. The newly formed virions need to break from the receptors they are attached to hence the neuraminidase breaks these receptors releasing the virus to go on and infect other cells.

Influenza A
•Influenza B
•Influenza C

27
Q

Type A viruses are divided into types based on differences in what?
Influenza type A viruses undergo two kinds of changes:
Name them

Influenza type B viruses change only by the more gradual process of antigenic drift. Type C infection usually causes either a very mild respiratory illness or no symptoms at all; True or false

A

two viral surface proteins called the hemagglutinin (H) and the neuraminidase (N).

Antigenic drift
Antigenic shift

True

28
Q

State six signs and symptoms of influenza

Although anybody can contract influenza infection, the majority of people with the illness are able to recover at home without the need for hospitalization or medical care. Most affected people make a full recovery within a week.
However, there are certain groups of people who are at higher risk of developing flu-related complications
True or false
Which five groups of people are at a higher risk of influenza
State six medical conditions which can increase your risk of flu related complications developing

A
Fever (usually 100F – 103F in adults and often even higher in children)
•Cough
•Sore throat
•Runny or stuffy nose
•Headache
•Muscle aches
•Extreme fatigue

True
. Such groups include:
•Adults over the age of 65
•Children under the age of five, in particular under the age of two
•People living in closed environments such as nursing homes or other care facilities
•Pregnant people and people up to two weeks after giving birth
•People with certain pre-existing medical conditions

Medical conditions which may increase the risk of flu-related complications developing include:

•Asthma
•Diabetes
•Heart diseases, such as heart failure and coronary artery disease
•Lung conditions, such as cystic fibrosis and bronchitis
•Kidney problems, such as chronic nephritic syndrome
•Liver disorders, such as hepatitis and cirrhosis
•Severe anemia
•Severe obesity, classified with a Body Mass Index (BMI) of 40 or higher
Medical conditions or treatments that can result in a weakened immune system, such as HIV infection or chemotherapy

29
Q

How is Influenza spread
State five lab investigations used to diagnose it
How is a sera diagnosis of influenza a and B made
Diagnosis for flu is based on the full medical history of the patient coupled with the laboratory investigations true or false

A

Influenza is spread mainly from person to person by droplet infection or droplet nuclei created by sneezing, coughing, or talking.

The portal of entry of the virus is the respiratory tract.

Virus Isolation
•Reverse Polymerase Chain Reaction (RT-PCR)
•Serology
•Rapid Antigen Testing
•Rapid Influenza Diagnostic Test
•Paired Sera

A sera diagnosis of influenza A and B can be made by the examination of two serum specimens from a patient.

True

30
Q

State four ddx of influenza

What are the complications of influenza (state that they’re grouped into two. Moderate and severe)

A
RSV Infection (Respiratory Syncytial Virus)
•Dengue fever
•Acute Respiratory Syndrome (ARDS)
•Bronchitis
•Histoplasmosis

Moderate
Moderate complications that can arise from influenza infection include:

  • Sinus infection, also known as sinusitis
  • Certain types of ear infection, such as acute otitis media
  • Young children may experience fits caused by the fever, known as febrile seizures

Severe
•Pneumonia
•Death

31
Q

How is influenza treated

A

At-Home Treatment
•Increasing liquid intake, warm showers, and warm compresses, especially in the nasal area, can reduce the body aches and reduce nasal congestion.

  • Nasal strips and humidifiers may also reduce congestion, especially while trying to sleep.
  • Fever can be treated with over-the counter acetaminophen (Tylenol) or ibuprofen (Motrin and others)

Antiviral medication
The most common antiviral medications used are:

  • Oseltamivir, typically swallowed as a pill or liquid
  • Zanamivir, typically inhaled as a powder
  • Peramivir, typically injected as a liquid
32
Q

State three ways influenza is prevented
What is Ebola
What causes it

A

Vaccine
The “flu shot” – an inactivated vaccine (containing killed virus) that is given with a needle, usually in the arm.

  • The nasal-spray flu vaccine – a vaccine made with live, weakened flu viruses that is given as a nasal spray (sometimes called LAIV for “Live Attenuated Influenza Vaccine”).
  • Practicing good personal hygiene can also help prevent the spread of influenza infection.

Ebola, also known as Ebola virus disease (EVD) and Ebola haemorrhagic fever (EHF), is a viral haemorrhagic fever in humans and other primates, caused by Ebola virus.

Ebola Virus Disease (EVD) is caused by Ebola virus. It’s origin or how it started is unknown. Scientists believe that it’s animal-borne and most likely comes from bats, which transmit the virus to other animals and humans.

33
Q

What is the pathophysiology of Ebola

A

Pathophysiology
Ebola enters the patient through mucous membranes, breaks into the skin, or parenterally and infects many cell types, including monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and epithelial cells.
the incubation period may be related to the infection route (6 days for injection versus 10 days for contact).
Ebola virus migrates from the initial infection site to regional lymph nodes and subsequently to the liver, spleen, and adrenal gland. Although not infected by Ebola virus, lymphocytes undergo apoptosis resulting in decreased lymphocyte counts.
Hepatocellular necrosis occurs and is associated with dysregulation of clotting factors and subsequent coagulopathy.
Adrenocortical necrosis also can be found and is associated with hypotension and impaired steroid synthesis. Ebola virus appears to trigger a release of re-inflammatory cytokines with subsequent vascular leak and impairment of clotting ultimately resulting in multiorgan failure and shock.

34
Q

What are the four modes of transmission of Ebola virus

A

Ebola virus is not as contagious as common viruses, such as colds or the flu. It is not spread through air, water, or food.
The Ebola virus is spread through direct contact with:

  • Blood of a person infected with the virus.
  • Body fluids such as breast milk, stool, saliva, semen, sweat, urine, or vomit, of a person infected with the virus.
  • Objects, such as needles or syringes, that are contaminated with the virus
  • Animals, such as bats and primates, that are infected with the virus.
35
Q

What are the risk factors of Ebola

NB: Even an infected dead body can still spread the virus.
True or false

A

For most people, the risk of being infected with Ebola virus is extremely low. The risk increases if you;

•Travel to an area where known EVD outbreaks have occurred.
•Help take care of someone infected with the virus
•Have direct contact with a person infected with the virus.
True

36
Q

What are the primary signs and symptoms of Ebola
State three symptoms that occur at the late stage

Symptoms may appear anywhere from how many days after contact with the virus, with an average of how many days.

The course of the illness typically progresses from “dry” symptoms initially (such as aches and pains, and fatigue), and then progresses to “wet” symptoms (such as diarrhoea and vomiting) as the person becomes sicker.

A

primary signs and symptoms of Ebola often include some or several of the following:

  • Fever
  • Aches and pains, such as severe headache, and muscle and joint pain
  • Weakness and fatigue
  • Sore throat
  • Loss of appetite
  • Gastrointestinal symptoms including abdominal pain, diarrhoea, and vomiting
  • Unexplained haemorrhaging , bleeding or bruising

Other likely symptoms may include red eyes, skin rash, and hiccups (late-stage)

2-21days after contact with the virus with an average of 8-10days

37
Q

What are the physical exam findings you expect to see generally,in the skin,respiratory system,extremities,nervous system

A

Appearance of the patient

•Temperature
More than 80% of patients present with high-grade fever.
Fever is the most common presenting sign of Ebola virus infection

•Pulse

i. Tachycardia
ii. Relative bradycardia

Respiratory System
Signs of respiratory difficulty may be present such as;
i.Intercostal retractions
ii.Paradoxical breathing
iii.Nasal flare
iv.Tachypnea often precedes death during final hours of infection.

Skin
Maculopapular rash on the trunk, usually between the 5th and 7th day of the condition.

•Extremities
Oedema may be present

•Neurologic

i. Stupor
ii. Coma

38
Q

State five investigations used to diagnose Ebola

Diagnosing Ebola Virus Disease (EVD) shortly after infection can be difficult.

Diagnosis is therefore based on the physical examination and the laboratory investigations

A

Polymerase Chain Reaction (PCR)
It has the ability to detect low levels of Ebola virus
•Antibody-capture Enzyme-linked Immunosorbent Assay (ELISA)
•Antigen-capture detection test
•Serum neutralization test
•Electron microscopy

39
Q

State four ddx if Ebola

An infectious disease in one country is a threat to all
•Important role of air travel in international spread
•Tremendous negative economic impact on trade, travel and tourism
•High level commitment is crucial for rapid containment
•WHO can play a crucial role in catalyzing international cooperation and support.

While dengue and chikungunya are insect-borne viral diseases, malaria, on the other hand, is caused by a parasite called Plasmodium. Malaria is associated with the Anopheles mosquito, whereas the other two diseases are caused due to an infection spread by the Aedes mosquito . While Chikungunya is caused by a Togaviridae alphavirus, Dengue is caused by a Flavirideae flavivirus.
True or false

A

Chikungunya fever: Chikungunya is characterized by an abrupt onset of fever, frequently accompanied by joint pain. The joint pain is often very debilitating. viral infection transmitted by mosquitoes.

•Dengue fever
•Typhoid fever
•Zika virus disease: disease caused by Zika virus that is spread through mosquito bites.
In most cases, there are no symptoms. In a few cases, Zika can trigger paralysis (Guillain-Barré Syndrome). In pregnant women, it may cause subsequent birth defects. Zika virus disease is caused by a virus transmitted primarily by Aedes mosquitoes, which bite during the day. ·
•Yellow fever disease: High Yellow fever is caused by a virus that is spread by the Aedes aegypti mosquito. fever returns and several body systems are affected, usually the liver and the kidneys. In this phase people are likely to develop jaundice (yellowing of the skin and eyes, hence the name ‘yellow fever’), dark urine and abdominal pain with vomiting. Bleeding can occur from the mouth, nose, eyes or stomach.
•Malaria

40
Q

How is Ebola treated

A

Whether or not other treatments are available, basic interventions can significantly improve chances of survival when provided early. These are referred to as supportive care, and they include:

  • Providing fluids and electrolytes (body salts) orally or through infusions into the vein (intravenously)
  • Using medication to support blood pressure, reduce vomiting and diarrhea, and to manage fever and pain.
  • Treating other infections, if they occur.

Pharmacological Treatment
There’s no cure for Ebola, though researchers are working on it. There are two drug treatments which have been approved for treating Ebola.

  • The U.S. Food and Drugs Administration approved Inmazeb, a mixture of three monoclonal antibodies (atoltivimab,maftivimab, and odesivimab-ebgn) as the first FDA approved treatment for Ebola virus infection in adult and pediatric patients.
  • Ansuvimab-zykl (Ebanga) is a monoclonal antibody given as an injection. It helps block the virus from the cell receptor, preventing its entry into the cell.
41
Q

What do you expect to see on chest x ray jn heart failure

A

A- alveolar edema ( appear like bats wings on both sides of upper heart)
B- Kerley B lines (interstitial edema and costophrenic angles)
C- cardiomegaly
D- dilated prominent upper lobe vessels
E- pleural effusion

42
Q

What is a stroke , state the types of stroke,

Brain stem stroke
Cerebellar stroke
Thalamic stroke
Basal ganglia stroke
Internal capsule stroke
What is a lacunar stroke?
What is the difference between Cortical Strokes vs Subcortical Strokes

A

A stroke occurs when the supply of blood in the brain becomes compromised. This can happen by either a blood clot obstructing an artery and stopping blood flow to an area of the brain (called an ischemic stroke) or an artery in the brain bursting and leading to bleeding inside the brain (called a hemorrhagic stroke).
Or it is a sudden focal neurological deficit resulting from spontaneous haemorrhage or infarction of CNS

The cerebral cortex/cerebrum is a large part of the brain that includes 4 lobes: the frontal lobe, parietal lobe, occipital lobe, and temporal lobe. Strokes in these regions are known as a cortical strokes.

Aside from the cerebrum, there are subcortical structures that lie deep within the brain. Strokes in these areas of the brain are also known as subcortical strokes. Arteries supplying this sub cortical structures are small and can easily be damaged or ruptured by high blood pressure leading to haemorrhahic stroke

When an ischemic stroke occurs in the subcortical regions, it’s referred to as a lacunar stroke.

43
Q

state the signs of stroke you will see when the lesion is in the : Frontal lobe stroke
Parietal lobe stroke

A

Effects of a frontal lobe stroke (a type of cortical stroke) include motor impairments, problem solving and judgement issues, behavioral changes, and difficulty with speech (aphasia, dysarthria, or apraxia of speech), among others.

A parietal lobe stroke mostly affects sensory interpretation along with language skills and spatial awareness. Some secondary effects of this cortical stroke include hemineglect, difficulty writing (agraphia), difficulty reading (alexia), difficulty speaking (aphasia), and more.

44
Q

state the signs of stroke you will see when the lesion is in the
Temporal lobe stroke
Occipital lobe stroke

A

The temporal lobe, also part of the cerebrum, is an area of the brain that controls language comprehension, hearing and other sensory processes. A temporal lobe stroke may affect hearing, vision, and speech comprehension, along with other secondary effects.

The occipital lobe, the final type of cortical stroke, plays a large role in your vision. As a result, and occipital lobe stroke often results in vision difficulties like central vision loss, cortical blindness, visual hallucinations, or other secondary effects.

45
Q

state the signs of stroke you will see when the lesion is in the brain stem and cerebellum

A

The brain stem is comprised of the midbrain, pons, and medulla oblongata. A stroke in any of these areas is considered a brain stem stroke.

The brain stem controls basic body functions like breathing, sweating, and consciousness. Therefore, common changes caused by a brain stem stroke include coma, difficulty breathing, and difficulty swallowing (dys

A stroke in the cerebellum is called a cerebellar stroke. The cerebellum controls some sensory functions and voluntary movements (especially balance and coordination). Effects of a cerebellar stroke may include ataxia, balance issues, and sensory issues, among others.

46
Q

state the signs of stroke you will see when the lesion is in the basal ganglia and left and right hemisphere

A

The basal ganglia are most associated with emotion, voluntary muscle control, cognitive function, and memory. Therefore, basal ganglia strokes often result in emotional blunting, post-stroke depression, and motor impairments, among other effects.

Generally speaking, the left hemisphere controls language and logical reasoning; while the right hemisphere is believed to control creativity and object recognition. This is why language difficulties after stroke are often associated with left hemisphere strokes.

Furthermore, each hemisphere controls movement on the opposite side of the body. Usually, a left hemisphere stroke will cause motor impairments on the right side of the body; while a right hemisphere stroke will likely impair the left side of the body.

47
Q

State the risk factors of stroke
What’s the difference between hemiplegia and Hemiparesis

A

Modifiable and non modifiable

Modifiable-
High blood pressure, heart disease such as AFib, heart failure and infective endocarditis, DM, hyperlipidemia, smoking, excess alcoholic consumption, polycythemia, oral contraceptives,

Non modifiable:
Age, sex ( common in males than females), race, heredity, previous vascular event such as MI or stroke or PE, high fibrinogen
Sickle cell and cyanotic congenital heart disease are risk factors in kids

Hemiplegia: Complete prarlysis on one side
Hemiparesis; partial weakness on one side

48
Q

State six causes of stroke and their respective investigations

State the investigations done for stroke

Neck stiffness or neck pain is a likely subarachnoid haemorrhage

A

Atherosclerosis- lipid profile
Systemic lupus erythematosis - antinuclear antibodies
Aortic dissection - angiography
Drug misuse- drug screen for cocaine and amphetamine
Coagulopathy- clotting profile
CT scan of the skull, ECG cause risk factor of stroke is cardiac problems , echocardiogram
Lumbar puncture to check if it’s a subarachnoid haemorrhage and not a stroke, blood glucose cuz DM can cause stroke ,

Other causes of stroke- obesity, smoking, arterio venous cerebral malformations(do MRI), HPT, sickle cell, DM, blood thinners, AFib, anti platelet drugs, valve diseases such as rheumatic heart disease, hormonal therapy

CT of skull to check for h or I stroke
LFT
RFT -Kidney disease is prevalent among stroke patients and may be associated with increased risk for recurrent stroke and poorer long-term outcomes.
HbA1C
Urine R/E
ECG
FBC- polycythemia or high WBcs can lead to hypercoaguble state which can lead to stroke . Leukemia can cause stroke
Blood glucose
BUE
Chest x ray

49
Q

State five complications of acute stroke and how you prevent and treat each of them
What are you concerned ahout when givinf warfarin?

A

Chest infection - prevent this by inserting NG tube to prevent aspiration . Treat antibiotics and chest physiotherapy

Epileptic seizures- prevent by avoiding metabolic disturbance and treat anticonvulsant

DVT- prevent by maintaining hydration, early mobilization and thromboembolism deterrent stockings or compression stockings
heparin for high risk patients and treat by giving anticoagulant but exclude haemorrhagic stroke first

Pressure sores-
Prevention by frequent turning, monitor pressure areas
Treat by adequate nursing care and pressure relieving mattress

UTI-
Treatment by antibiotics

Depression- prevent by providing information and maintaining positive attitude. Treat by giving anti depressants

Warfarin for first two days has pro thrombic effect so you give with Clexane . So you check INR after three days of the warfarin Clexane therapy then if it’s 2-3, stop the Clexane .
Also AFib is not a diagnosis it is always secondary to something

50
Q

How is stroke managed
What will you counsel the patient on discharge?

A

Do ABCs
Airway- check if airway is patent and if patient can swallow. Suction if any secretions ,
Breathing- check if breathing is adequate, oxygen saturation , respiratory rate and give oxygen is saturation is less than 95%

Circulation- wide bore cannulas and take blood samples for investigations, give IV fluids for hydration , check the pulses and blood pressure and capillary refill
Admit and Vitals and neurological signs monitoring 4 hourly
Control BPs if high
Elevate the head ( to 30 degrees to reduce ICP) and turn patient every 2 hours. Make sure bed sheet is straight to reduce pressure sores,
pass NGt tube if they can’t swallow . Do swallow test in upright position using 10-15mls of water
Pass catheter if unconscious
Treat the underlying cause
Identify and Treat infections
Thromboembolic deterrent stockings to prevent dvt
Adequate nutrition
Physiotherapy
Refer

Pharmacological:
InfarctiVe and TIAs
Give dvt prophylaxis if it’s confirmed that it’s an InfarctiVe stroke
Aspirin 300mg stat then 75mg daily.
Atovastatin 40-80mg oral

Haemorrhagic stroke with evidence of cerebral edema :
IV mannitol ( make sure you hydrate adequately when giving mannitol to prevent AKI)

Control co morbidities such as hpt , diabetes if present

Start:
History and exam- to identify risk factors site and extent of stroke and sources of the embolism
Investigations
Hydration using NS or DNS. 2.5-3L per day. Give 5% and 10% dextrose only if hypoglycemic
Give proton pump inhibitor for stress ulcer prophylaxis
Control the glucose by keeping RBs 4-10mmol/L, insulin sliding scale. Avoid oral metformin if diabetic
Pyrexia- if more than 37,5 am she with para and consider the source and act accordingly
Manage blood pressure - if it’s more than 180/110 aim for gradual reduction 20% over 24 hours . Sudden drop can extend stroke
Treat infarcts using 300mg aspiring if no contraindications. Reduce to 75 after one week
Afib- rhythm control ABCD
Mobilize patients by early referral to physio even if patient is unconscious
Aspiration pneumonia- look for signs of this regularly such as rising RR, tachycardia and chest signs. Treat with IV amoxicillin +clavulanic acid and IV metronidazole for first 48hours and review
Seizures- terminate per protocol and give anticonvulsant if more than one occurs
High cholesterol- statins
Rising ICP - elevate head and give IV mannitol
Change in conscious level- consider cerebral edema, hypoglycemia, metabolic and drug causes that can be reversed

Counsel-
Counsel patient on good nutrition
Cojnsel oatient on exercise
Counsel patient on smoking cessstion

51
Q

State five risk factors for dvt and three causes of dvt

A

Risk factors- pregnancy, obesity, prolonged immobilization, hypercoaguble state, major surgery such as an orthopedic surgery, oestrogen therapy, CCF, MI, Nephrotic syndrome, stroke , systemic lupus erythematosis

Causes- stagnation of blood in vein, increased viscosity of blood, inflamed blood vessel

52
Q

State three signs and symptoms and three jnvestigations for dvt

A

Symptoms- swelling of affected limb
Pain in affected limb, mild fever, intermittent claudication

Sign- swelling of aff ex red limb, differential warmth, tenderness, redness, prominent superficial veins, putting edema

Investigations-
D dimer, Doppler ultrasound, FBC( to check platelets), thrombophilis screen for protein C and S levels in patients with recurrent dvt

53
Q

What is the Wells scoring for DVT probability and it’s interpretation

A

This objectified clinical suspicion of DVt risk and provides criteria for imitating treatment

Paralysis, paresis or recent orthopaedjc casting of lower extremity 1 point
Recently bedridden rn more than three days or major surgery in past four weeks 1 pojnt
Localized tenderness in deep vein system 1 point
Swelling of entire leg (1 point)
Calf swelling 3 cm created than other leg( measured 10 cm below tuberal tuberosity) 1 point
Putting edema greater in symptomatic leg 1 point
Collateral non varicose supeficak veins 1 pint
Active cancer or cancer treated within 6 months 1 point
Alternative diagnosis more likely than DVT ( bakers cyst, cellulitis, muscle damage, superficial vein thrombosis, external venous compression) 2 points

Interpretation-
3-8 points is high prob of dvt( d dimer with Doppler or compression ultrasound)
1-2 moderate prob
0 below low prob( d dimer )

54
Q

How is dvt and PE managed
You don’t give warfarin in pregnancy why ?

A

Non pharmacological :
Avoid dehydration and prolonged lying down
Avoid excess amounts of coffee and alcohol especially on long journeys
Increase water intake during long periods of immobility
Regular exercise
Use of elastic thromboembolic deterrent stockings

Pharmacological:
First line is Sc heparin

Second line is enoxaparin SC

PE:
Non Pharma- elevate affected leg on pillow of dvt is present
Apply compression stockings

Pharma-
Give oxygen and morphine then give enoxaparin SC

Warfarin is a teratogen which can cross from the mother to the developing fetus. The inhibition of clotting factors can lead to internal bleeding of the fetus while the inhibition of osteocalcin causes lower bone growth. As well as birth defects, warfarin can induce spontaneous abortion or stillbirth.

Use of warfarin in pregnancy can cause bleeding behind the placenta. This type of bleeding can cause reduced fetal growth, placental abruption, and stillbirth (if severe). The chance of preterm delivery is also higher.

55
Q

State five investigations in PE
Explain the Wells score for PE probability and interpretation for PE

A

D dimer
Doppler ultrasound of affected limbs
Chest C ray
FBC
ECG
Echo

Scoring:
Symptoms of DVT 3point
No alternative diagnosis better explains illness 3 points
Tachycardia with pulse more than 100bpm 1.5points
Immobilization for more than three days or surgery in previous four weeks 1.5 points
Prior history of DVt or pulmonary embolism 1.5 points
Presence of hemoptysis 1 point
Presence of malignancy 1 point

Interpretation:
More than 6 high probability
More than or equal to 2 but less than or equal to six moderate probability(d dimer with CT pulmonary angiography is recommended. Same for high probability)
Less than 2 low probability (D dimer test is recommended)

56
Q

State the signs and symptoms of PE

A

Symptoms
Dyspnea
Chest pain
Cough
Hemoptysis
Syncope
Unilateral swelling

Signs:
Tachypnea
Tachycardia
Low BP
Pleural effusion
Low O2
Cyanosis
Unilateral swollen calf or thigh

57
Q

What is ACS
State four risk factors and one cause of ACS
What is Ischemic heart disease
How does stable angina present or myocardial ischemia present ( use Socrates to explain)
And how is stable angina treated
Avoid atenolol in heart failure. (However, in heart failure patients, atenolol can increase the end-diastolic pressure and left ventricular fiber lengths - conversely resulting in increased oxygen demand.)

A

A term that describes symptoms resulting from severe acute myocardial ischemia and it may or may not lead to an MI or heart attack
ACS is STEMI, nonstemi and unstable angina( ACS without elevation of cardiac enzymes)

Risk factors- obesity, DM, hypertension, smoking, hyperlipidemia

Cause/ atherosclerosis or obstruction of coronary blood vessels leading to reduced blood supply to heart muscle.
So a myocardial ischemia May or may not lead to a myocardial infarction

Ischemic heart disease or coronary artery disease comprises of stable angina and ACS due to reduced blood flow to heart muscle to do atherosclerosis.

Stable angina or myocardial ischaemia presents as central chest pain with tightening or crushing or heaviness and is relieved by rest. It may radiate to the neck jaw teeth or arms. Precipitate include anxiety, emotions, cold weather and heavy meals. It is also relieved by glyceryl trinity are. Pain commonly radiates to left arm jaw or neck or shoulder. There can be dyspnea nausea sweating associated with the pain

Treatment:
Lifestyle changes and treat risk factors such as DM and HPt
Pharmacological- glyceryl nitrate (relaxes blood vessels and widens them) sub lingual(means under tongue) , either aspirin or clopidogrel 300mg stat, beta blockers such as atenolol, if beta blockers or verapamil is contraindicated, give isosorbide dinitrate ( relaxes blood vessels )
If high cholesterol, give a statin

58
Q

What will you see in NONSTEMI ECG
State the signs and symptoms of ACS

A

NONSTEMI ECG- ST depression, T wave inversion, non specific changes or may be normal

Symptoms are same as Stable angina
Acute central chest pain lasting more than 20mins associated with nausea sweating vomiting exertional dyspnea relieved by rest ,palpitations. Can present in elderly and DM as syncope stroke or pulmonary edema without the chest pain and is a silent infarct
Epigastric pain and vomiting

Signs- bradychardia
Tachypnoea
High or low bp
Sweating
Distress
Distended jvp
Signs of heart failure may be present

59
Q

State six investigations and five differentials for ACS

A

Investigations
ECG
LIPID PROFILE
CHEDT X RAY
FBC
BUE
CARDIAC ENZYMES
RBs cuz DM are at risk of this
Echo
CT angiography

differentials- Angina, pericarditis, myocarditis, aortic dissection, pulmonary embolism , GERd

60
Q

How is ACS managed:

Acute coronary syndrome (ACS, formerly called ischemic heart disease) refers to a large spectrum of clinical conditions including unstable angina, myocardial injury, and myocardial infarction (MI). ACS is caused by a sudden onset of cardiac tissue ischemia secondary to impaired blood flow. So the mgt in ACs is more than in stable angina because ACS is an emergency and stable angina isn’t

A

ABcs
Give oxygen
Oral aspirin 300mg stat
Oral clopidogrel 300mg stat
Glyceryl nitrate sub lingual
Morphine IV
Metoclopramide IV ( to prevent vomiting induced by morphine)
All the above medications stat

When stabilized, refer if in health center to physician specialist

Maintenance after initial treatment
Lower apsirin and clopidogrel to 75mg
Give anticoagulant enoxaparin SC
Give atenolol and Lisinopril to reduce myocardial workload and prevent arrhythmias
Manage acute complications such as shock and pulmonary edema
Manage hyperglycemia with insulin and change diabetic patients previously on oral hypoglycaemic agents to insulin
Atovastatin to reduce blood cholesterol levels