Anaemia And Pneumonia Flashcards
What is Anaemia?
What is Hb,Hct,RBcs
What 3 things does the degree to which a patient become symptomatic depend on?
When do most patients experience some symptoms related to anemia?
Anemia is a reduction in hemoglobin (Hb) or hematocrit (HCT) or RBC count
•Anemia is not a diagnosis, but a presentation of an underlying condition.
•Whether or not a patient becomes symptomatic depends on the etiology of anemia, the acuity of onset, and the presence of other comorbidities, especially the presence of cardiovascular disease.
•Most patients experience some symptoms related to anemia when the hemoglobin drops below 7.0 g/dL.
Reduction in the volume of RBC’s (hematocrit) or concentration (hemoglobin) when compared to similar values from a reference population.
•Hgb = expression of amount (g/dL).
•Hct = expression of volume (% or decimal fraction).
•RBC = expression of number (#/mm3).
What are the normal Hb levels for men, women and kids?
How does RBc production occur?
What things prevent RBC production
Normal Hemoglobin (Hgb)-specific laboratory cut-offs will differ slightly, but in general, the normal ranges are as follows:
•13.5 to 18.0 g/dL in men
•12.0 to 15.0 g/dL in women
•11.0 to 16.0 g/dL in children
•Varied in pregnancy depending on the trimester, but generally greater than 10.0 g/dL
Myeloid stem cells turn to erythroblasts turn to reticulocyte (immature RBCs) then turn to erythrocyte
RBc production occurs in red bone marrow. In red bone marrow there is myeloid stem cell which can become an RBC,WBC or platelet.
Hormonal stimulants drive RBc production- stimulants such as thyroid hormones, erythropoietin (from kidneys and liver), Iron-B12-Folate from GIT
Toxins and alcohol suppress bone marrow
Intrinsic problems with bone marrow function- cancer of bone marrow cells can reduce RBcs, chemo radiation destroying intrinsic bone marrow
State and explain the three main mechanisms of Anaemia(State ten causes of Anaemia)
What happens when RBcs are low?
Blood loss
•Acute- hemorrhage, surgery, trauma, menorrhagia(heavy menstrual bleeding)
•Chronic-, chronic gastrointestinal blood losses [6] (in the setting of hookworm infestation, ulcers, etc.), urinary losses (BPH, renal carcinoma, schistosomiasis)
Hemolytic anemia
•Acquired- immune-mediated, infection, microangiopathic, blood transfusion-related, and secondary to hypersplenism
•Hereditary- enzymopathies, disorders of hemoglobin (sickle cell), defects in red blood cell metabolism (G6PD deficiency, pyruvate kinase deficiency), defects in red blood cell membrane production (hereditary spherocytosis and elliptocytosis)
Intravascular-Intravascular hemolysis occurs in hemolytic anemia due to the following:
Prosthetic cardiac valves
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Thrombotic thrombocytopenic purpura
Disseminated intravascular coagulation
Transfusion of ABO incompatible blood
Paroxysmal nocturnal hemoglobinuria (PNH)
COVID-19 [4, 5]
Pyruvate kinase deficiency [6]
Extravascular-Autoimmune hemolytic anemia and hereditary spherocytosis are examples of extravascular hemolysis because the red blood cells are destroyed in the spleen and other reticuloendothelial tissues. [3]
Deficient/defective erythropoiesis (hypoproliferative anaemia)
•Microcytic
•Normocytic, normochromic
•Macrocytic
When RBcs are low, they make the myeloid stem cells produce more RBCs if the bone marrow is working properly
State five conditions under each hypoproliferative Anaemia
What is the MCV (mean corpuscular volume which shows the sizes of the RBCs) for each type?
Macrocytic Anaemia can be caused by either what or what?
How will you know what is causing the macrocytic Anaemia
What drugs cause normocytic anaemia?
How will you differentiate megaloblastic Anaemia from non megaloblastic anaemia?
1) Hypoproliferative Microcytic Anemia (MCV<80 fl(femtolitres)
•Iron deficiency anemia
•Anemia of chronic disease (AOCD)
•Sideroblastic anemia (may be associated with an elevated MCV as well, resulting in a dimorphic cell population)
•Thalassemia
•Lead poisoning( which can also cause sideroblastic Anaemia)
Causes
2)Hypoproliferative Normocytic Anemia (MCV 80-100 fL)
•Anemia of chronic disease (AOCD)
•Renal failure
•Aplastic anemia
•Pure red cell aplasia
•Myelofibrosis or myelophthisic processes
•Multiple myeloma
Hypoproliferative Macrocytic Anemia (MCV>100 fL)
•Alcohol
•Liver disease
•Hypothyroidism
•Folate and Vitamin B12 deficiency [3]
•Myelodysplastic syndrome (MDS)
•Drug-induced ( chemo drugs, anti seizure meds, TB meds , HIV meds, some antibiotics
Macrocytic anemia can be caused by either a hypoproliferative disorder, hemolysis, or both.
•Thus, it is important to calculate the corrected reticulocyte count when evaluating a patient with macrocytic anemia.
•In hypoproliferative macrocytic anemia, the corrected reticulocyte count is <2%, and the MCV is greater than 100 fl.
•But, if the reticulocyte count is > 2%, hemolytic anemia should be considered
So under macrocytic Anaemia we have megaloblastic and non Megaloblastic
Megaloblastic have hypersegmented PMN on peripheral blood smear or blood film but Non megaloblastic have hyposegmented PMN on peripheral blood smear or blood film
Megaloblastic anaemia suggest Iron deficiency, B12,folate deficiency, alcohol, medications causing the Anaemia
Haemolytic Anaemia is divided into two
State, define and give examples of each
Hemolytic anemia (HA) is divided into extravascular and intravascular causes
•Extravascular hemolysis: red cells are prematurely removed from the circulation by the macrophages in the liver and spleen. This accounts for a majority of cases of HA
•Hemoglobinopathies (sickle cell, thalassemias)
•Enzyemopathies (G6PD deficiency(G6PDH reduces oxidative stress on RBcs and since it’s not present, oxidative stress causes RBc to lose their integrity making them likely to taken by the macrophages in the liver or spleen when blood with such RBCs pass through these organs) , pyruvate kinase deficiency)
•Membrane defects (hereditary spherocytosis, hereditary elliptocytosis)
•Drug-induced
Intravascular hemolysis: red cells lyse within the circulation, and is less common.
•PNH(paroxysmal nocturnal haemoglobinuria)
•AIHA
•Transfusion reactions
•MAHA(microangiopathic Haemolytic Anaemia)
•DIC
•Infections
•Snake bites/venom
What questions will you ask on history?
(Ask in accordance to the three mechanisms of Anaemia or causes of Anaemia)
A thorough history and physical must be performed.
•Some important questions to obtain in a history:
•Obvious bleeding- per rectum or heavy menstrual bleeding, black tarry stools, hemorrhoids
•Thorough dietary history
•Consumption of nonfood substances
•Bulky or fatty stools with foul odor to suggest malabsorption
•Thorough surgical history, with a concentration on abdominal and gastric surgeries
•Family history of hemoglobinopathies, cancer, bleeding disorders
•Careful attention to the medications taken daily
:
State five signs and symptoms each of Anaemia
How does permicious Anaemia occur?
Classically depends on the rate of blood loss. Symptoms usually include the following:
•Weakness
•Tiredness
•Lethargy
•Restless legs
•Shortness of breath, especially on exertion, near syncope
•Chest pain and reduced exercise tolerance- with more severe anemia
•Pica- desire to eat unusual and nondietary substances
•Mild anemia may otherwise be asymptomatic
Skin may be cool to touch
•Tachypnea
•Hypotension (orthostatic)
•Pallor of the conjunctiva
•Jaundice- elevated bilirubin is seen in several hemoglobinopathies, liver diseases and other forms of hemolysis
•Lymphadenopathy: suggestive of lymphoma or leukemia
•Glossitis (inflammation of the tongue) and cheilitis (swollen patches on the corners of the mouth): iron/folate deficiency, alcoholism, pernicious anemia
Pernicious anemia is a type of vitamin B12 anemia. The body needs vitamin B12 to make red blood cells. You get this vitamin from eating foods such as meat, poultry, shellfish, eggs, and dairy products.
A special protein, called intrinsic factor (IF), binds vitamin B12 so that it can be absorbed in the intestines. This protein is released by cells in the stomach. When the stomach does not make enough intrinsic factor, the intestine cannot properly absorb vitamin B12.
Common causes of pernicious anemia include:
Weakened stomach lining (atrophic gastritis)
An autoimmune condition in which the body’s immune system attacks the actual intrinsic factor protein or the cells in the lining of your stomach that make it.
On abdominal exam, what are signs of anemia seen and what may cause it?
How does Anaemia affect the CVS
Abdominal exam
•Splenomegaly: hemolysis, lymphoma, leukemia, myelofibrosis
•Hepatomegaly: alcohol, myelofibrosis
•Scar from gastrectomy: decreased absorptive surface with the loss of the terminal ileum leads to vitamin B12 deficiency
•Scar from cholecystectomy: Cholesterol and pigmented gallstones are commonly seen in sickle cell anemia are hereditary spherocytosis
Cardiovascular
•Tachycardia
•Systolic flow murmur
•Severe anemia may lead to high output heart failure
How do you evaluate Anaemia (think about for each type of Anaemia)
Start from the top
How is reticulocyte count calculated?
How Is the value gotten interpreted
What normal HCT for men and women to claukate the reticulocyte count
Evaluation
•Complete blood count (CBC) including differential
•Calculate the corrected reticulocyte count = percent reticulocytes x (patient’s HCT/normal HCT)
•For normal HCT, use 45% in men and 40% in women
•If result > 2, this suggests hemolysis or acute blood loss, while results < 2 suggests hypoproliferation.
How is microcytic Anaemia evaluated?
After calculating the reticulocyte count, check the MCV.
MCV (<80 fl)
•Iron deficiency- decreased serum iron, percent saturation of iron, with increased total iron-binding capacity (TIBC), transferrin levels, and soluble transferrin receptor, decreased ferritin levels
•Lead poisoning- basophilic stippling on the peripheral blood smear, ringed sideroblasts in bone marrow, elevated lead levels
•Thalassemia- RBC count may be normal/high, low MCV, target cells, and basophilic stippling are on peripheral smear. Alpha thalassemia is differentiated from beta-thalassemia by a normal Hgb electrophoresis in alpha thalassemia. Elevated Hgb A2/HgbF is seen in the beta-thalassemia trait.
•Sideroblastic anemia- elevated serum iron and transferrin with ringed sideroblasts in the bone marrow
How is normocytic Anaemia evaluated
Evaluation
•MCV (90-100fl)
•Renal failure: BUN/Creatinine
•Aplastic anemia- ask for drug exposure, check for infections (EBV, hepatitis, CMV, HIV), test for hematologic malignancies and paroxysmal nocturnal hemoglobinuria (PNH)
•Myelofibrosis/myelophthisis- check bone marrow biopsy
•Multiple myeloma- serum and urine electrophoresis
Macrocytic Anaemia evaluated
MCV (>100 fl)
•B12/folate levels- B12 and folate deficiency can be differentiated by an elevated methylmalonic and homocysteine level in B12 deficiency and only an elevated homocysteine level in folate deficiency. Methylmalonic levels are relatively normal.
•MDS- hyposegmented PMNs on peripheral smear, bone marrow biopsy
•Hypothyroidism- TSH, free T4
•Liver disease- check liver function
•Alcohol- assess alcohol intake
•Drugs
How do you evaluate Haemolytic Anaemia
Bite cells on PBS indicate what?
Target cells on PBS indicate what?
Schistocytes on PBS indicate what?
Acanthocytes on PBS indicate what?
State three other investigations that may be needed
Steps to evaluate for hemolytic anemia
•Confirm the presence of hemolysis- elevated LDH, corrected reticulocyte count >2%, elevated indirect or unconjugated bilirubin
•Examine the peripheral blood smear
•Spherocytes: immune hemolytic anemia (Direct antiglobulin test DAT+) vs. hereditary spherocytosis (DAT-)
•Bite cells: G6PD deficiency
•Target cells: hemoglobinopathy or liver disease
•Schistocytes: TTP/HUS, DIC, prosthetic valve, malignant HTN
•Acanthocytes: liver disease
•Parasitic inclusions: malaria, babesiosis, bartonellosis
Other investigations that might be warranted include:
•esophagogastroduodenoscopy for the determination of an upper GI bleed,
•colonoscopy for the determination of a lower GI bleed,
•imaging studies if malignancy, or internal hemorrhage is suspected.
•If a menstruating woman has heavy vaginal bleeding, evaluate the presence of fibroids with a pelvic ultrasound.
How are Anaemia due to nutritional deficiencies managed?
What are the common side effects of supplement iron
How long does it take for haemoglobin to normalize afte taking oral iron
Anemia due to nutritional deficiencies:
•Oral/IV iron, B12, and folate.
•Oral supplementation of iron is by far the most common method of iron repletion. The dose of iron administered depends on the patient’s age, calculated iron deficit, the rate of correction required, and the ability to tolerate side effects.
•The most common side effects include metallic taste and gastrointestinal side effects such as constipation and black tarry stools. For such individuals, they are advised to take oral iron every other day, in order to aid in improved GI absorption.
•The hemoglobin will usually normalize in (2 weeks earliest) 6-8 weeks, with an increase in reticulocyte count in just 7-10 days.
•IV iron may be beneficial in patients requiring a rapid increase in levels. Patients with acute and ongoing blood loss or patients with intolerable side effects are candidates for IV iron.
Management of anemia depends on what?
What is the target haemoglobin for most patients?
What is the target hamoglobjn for people with cardiovascular disease
Management depends primarily on treating the underlying cause of anemia.
•Anemia due to acute blood loss- Treat with IV fluids, crossmatched packed red blood cells, oxygen.
•Always remember to obtain at least two large-bore IV lines for the administration of fluid and blood products.
•Maintain hemoglobin of > 7 g/dL in a majority of patients.
•Those with cardiovascular disease require a higher hemoglobin goal of > 8 g/dL.
How is Anaemia due to defects in the bone marrow and stem cells managed?
How is anemia due to chronic disease managed?
Anemia due to defects in the bone marrow and stem cells: Conditions such as aplastic anemia require bone marrow transplantation.
•Anemia due to chronic disease: Anemia in the setting of renal failure, responds to erythropoietin. Autoimmune and rheumatological conditions causing anemia require treatment of the underlying disease.
How is Anaemia due to increased RBC destruction managed?
Anemia due to increased red blood cell destruction:
•Hemolytic anemia due to medications requires the removal of the offending drug.
•Persistent hemolytic anemia requires splenectomy.
•Hemoglobinopathies such as sickle anemia require blood transfusions, exchange transfusions, and even hydroxyurea to decrease the incidence of sickling.
•DIC, which is characterized by uncontrolled coagulation and thrombosis, requires the removal of the offending stimulus. Patients with life-threatening bleeding require the use of antifibrinolytic agents.
When do you send blood films in patients?
Why will you give vitamin C to patients with nutrient deficiencies
Always send blood films in patients with an unclear etiology of anemia.
•Start haematinics early (iron, B12, and folate).
•Inform patients of the side effects of iron therapy, including constipation and black, tarry stools.
•Consider screening for sickle cell and thalassemia in patients with unexplained anemia or with a family history of these diseases.
•Vitamin C aids iron absorption, so coadministration of vitamin C with iron, or encouraging the patients to take iron supplements with orange juice, will aid therapy.
State ten complications of Anaemia
Anemia, if undiagnosed or left untreated for a prolonged period of time can lead to multiorgan failure and can even death.
•Pregnant women with anemia can go into premature labor and give birth to babies with low birth weight
•Anemia during pregnancy also increases the risk of anemia in the baby and increased blood loss during pregnancy.
Complications are more predominant in the older population due to multiple comorbidities
•The cardiovascular system is the most commonly affected in chronic anemia. Myocardial infarction, angina, and high output heart failure are common complications. Other cardiac complications include the development of arrhythmias and cardiac hypertrophy.
•Severe iron deficiency is associated with restless leg syndrome and esophageal webs.
•Severe anemia from a young age may lead to impaired neurological development in the form of cognitive, mental, and developmental delays. These complications are unlikely to be amenable to medical management.
When do you do consultations with other departments?
Gastroenterologist if a gastrointestinal bleed is suspected
•Nephrologist if anemia of chronic disease in the setting of renal failure is suspected
•Hematologist if a bone marrow disorder is suspected
•Gynecologist if intractable menorrhagia is suspected
•Cardiologist if severe anemia leads to angina, myocardial infarction, heart failure, or arrhythmias
What is pneumonia
State the three different classes of pneumonia and explain one classification
State five organisms causing community acquired pneumonia and hospital acquired pneumonia
Inflammation of the lung parenchyma
It’s an acute respiratory illness
Three classes:
Classification by site of acquisition-
Community acquired pneumonia
Nosocomial pneumonia
Hospital acquired pneumonia
Ventilator associated pneumonia
Health care associated pneumonia
Classification by Aetiology:
Atypical pneumonia
Chemical pneumonitis
Bacterial aspiration pneumonia
Aspiration pneumonia
Classification by anatomy:
Lobar pneumonia
Bronchopneumonia
Interstitial pneumonia
Classification by site of acquisition-
Community acquired pneumonia : an acute infection of the pulmonary parenchyma acquired outside the hospital setting
Nosocomial pneumonia : an acute infection of the pulmonary parenchyma acquired in the hospital setting and it encompasses Hospital acquired pneumonia and Ventilator associated pneumonia
Hospital acquired pneumonia : pneumonia acquired more than ir equal to 48 hours after hospital admission it includes both HAP and VAP
Ventilator associated pneumonia : pneumonia acquired more than ir equal to 48 hours after endotracheal intubation
Health care associated pneumonia:it’s a retired term which refers to pneumonia gotten from health facilities (nursing home,haemodialysis centre) or after recent hospitalization
Community acquired pneumonia
y Streptococcuspneumonia
y Streptococcuspyogenes
y Haemophilusinfluenza
y Klebsiellapneumoniae
y Mycoplasma pneumonia and Legionella pneumophila (tend to occur in epidemics)
y Staphylococcus aureus (in children after viral illness like measles, in diabetics or in the elderly during ‘flu’ epidemics)
Hospital acquired pneumonia
y Gram-negative bacteria e.g. Pseudomonas aeruginosa
y MRSA (Methicillin resistant)
y VRSA (Vancomycin resistant)
y Staphylococcus aureus
Others
y Pneumocystis jiroveci pneumonia and other fungi (in immunocompromised states e.g. haematological malignancies, HIV/ AIDS)
y Viruses
State five bacteria that can cause atypical pneumonia and arxplain the classification of pneumonia by aetiology
Classification by Aetiology:
Atypical pneumonia -pneumonia caused by atypical bacteria pathogens including Legionella spp, mycoplasma pneumoniae, Chlamydia pneumoniae, Chlamydia psittaci and Coxiella burnetti
Chemical pneumonitis:aspiration of substances example acidic gastric fluid that cause an inflammatory reaction in the lower airways independent of bacterial infection
Bacterial aspiration pneumonia:an active infection caused by inoculation of large amounts of bacteria into the lungs via orogastric contents
Aspiration pneumonia: adverse pulmonary consequences due to entry of gastric or oropharyngeal fluids which may contain bacteria and or be of low pH or exogenous substances (infested food particles or liquids,mineral oils,salt and fresh water) into the lower airways
State five pathogen that cause pneumonia classifi by anatomy (gram
Positive, gram negative, viruses,atypical bacteria)
Gram negative: Klebsiella pneumoniae, haemophilus influenzae, Moraxella catarrhalis, E. coli
Positive: strep pneumoniae, Staph aureus, Group A haemolytic strept
Atypical bacteria: anaerobes, viral or fungal, legionella,Mycoplasma pneumoniae
Viruses: influenza A and B, SARS COV-2,RSV,Adenovirus
How do the symptoms of pneumonia occur?
Systemic cytokine release leads to dysregulation of the hypothalamic thermoregulation leading to fever and chills or rigors
In lobar pneumonia, accumulation of neutrophils and plasma exudate from capillaries into alveoli of specific area of the lung or lobes.
This leads to irritation and attempted clearance of the airways, the fluid infiltrates are inside the alveoli, airway clearance leads to phlegm production and this leads to a productive cough.
The accumulation into specific lobes also leads to fluid build up and this does not allow the X rays to pass through so there is white opacity on plain film at the site of the fluid build up. This shows as a consolidation on chest x ray
The accumulation of fluid in the lobes also lead to blockage of the alveolar sacs and this decreases exchange of CO2 and O2. This leads to hypoxemia and this triggers peripheral and central chemoreceptors to increase respiratory drive hence leading to dyspnea
In interstitial pneumonia, there is accumulation of infiltrates( inflamed cellular debris) in the alveolar walls (that is, space between the alveolar spaces and bloodstream)
This leads to thickening of the alveolar walls and increased diffusion distance between the alveoli and capillaries
this decreases exchange of CO2 and O2. This leads to hypoxemia and this triggers peripheral and central chemoreceptors to increase respiratory drive hence leading to dyspnea
Accusation of infiltrates also lead to irritated alveolar walls and triggers a cough reflex
Since fluid infiltrates are not in the alveoli, attempts to
Empty the alveoli by coughing doesn’t lead to production of fluid so there’s a dry cough
How do the symptoms of pneumonia occur?
Systemic cytokine release leads to dysregulation of the hypothalamic thermoregulation leading to fever and chills or rigors
In lobar pneumonia, accumulation of neutrophils and plasma exudate from capillaries into alveoli of specific area of the lung or lobes.
This leads to irritation and attempted clearance of the airways, the fluid infiltrates are inside the alveoli, airway clearance leads to phlegm production and this leads to a productive cough.
The accumulation into specific lobes also leads to fluid build up and this does not allow the X rays to pass through so there is white opacity on plain film at the site of the fluid build up. This shows as a consolidation on chest x ray
The accumulation of fluid in the lobes also lead to blockage of the alveolar sacs and this decreases exchange of CO2 and O2. This leads to hypoxemia and this triggers peripheral and central chemoreceptors to increase respiratory drive hence leading to dyspnea
In interstitial pneumonia, there is accumulation of infiltrates( inflamed cellular debris) in the alveolar walls (that is, space between the alveolar spaces and bloodstream)
This leads to thickening of the alveolar walls and increased diffusion distance between the alveoli and capillaries
this decreases exchange of CO2 and O2. This leads to hypoxemia and this triggers peripheral and central chemoreceptors to increase respiratory drive hence leading to dyspnea
Accusation of infiltrates also lead to irritated alveolar walls and triggers a cough reflex
Since fluid infiltrates are not in the alveoli, attempts to
Empty the alveoli by coughing doesn’t lead to production of fluid so there’s a dry cough
State the six ways pneumonia is diagnosed
State the presentation of pneumonia (pulmonary signs and symptoms and systemic signs and symptoms)
State the clinical exam findings on pneumonia
History
Physical exam
Stage severity
Risk factors
Investigations
Identify sequelae
Pulmonary signs and symptoms :
Cough with or without sputum production, dyspnea, pleuritic chest pain
Tachypnea,increased work of breathing, adventitious breath sound such as rales or crackles and Rhonchi
Increased tactile fremitus and dullness on percussion
Systemic signs and symptoms:
Fever chills fatigue malaise chest pain anorexia
How will you classify pneumonia according to chest x ray
How will you classify pneumonia according to chest x ray and state the organisms that usaully cause the type of pneumonia according to anatomy
Lobar pneumonia:
Homogenous consolidation, silhouette sign, air bronchogram, sharply marginated fissure
Organism- Strept pneumoniae
Bronchopneumonia:
Poorly defined Heterogenous patchy infiltrates scattered throughout the lungs, air bronchogram
Organisms: Staph aureus leading to multi lobar, cavitation, pneumatocoeles , abscess
Interstitial pneumonia:
Bilateral diffuse fine reticular opacity
Organism: pneumocystis jiroveci pneumonia (PCP)
Aspiration:
Airspace opacification in a lobar or segmental distribution
Gravity dependent predilection
Organism: stroke , seizure
State ten investigations for pneumonia and why you’d want those investigations
Pulse oximetry- low arterial oxygen saturation
FBC-leucocytosis WBC more than 12 x 10 /L indicates bacterial aetiology
CRP-elevated level more than 100 mg/L Makes pneumonia more likely
Microbiology-sputum culture and gram staining, blood culture, pleural fluid analysis ,COVID-19 testing
BUE and Cr-usually normal but urea may be elevated
Liver function test:usually normal, good for baseline measurement
Maybe abnormal in severed disease and sepsis
Arterial blood gas- low arterial oxygen saturation
Other imaging test: chest ct scan, chest ultrasound
Others: lactate(In patients with severe pneumonia, tissue organ effective blood volume reduction, which further exacerbates tissue hypoxia and increases anaerobic metabolism. Blood lactic acid is a product of the anaerobic glycolysis of glucose, and can directly reflect the tissue hypoperfusion and hypoxia conditions. ) ,
“procalcitonin (The final step in the synthesis of calcitonin is inhibited by cytokines and endotoxin released during bacterial infections; therefore, procalcitonin levels are selectively elevated in patients with bacterial infections.. Procalcitonin has good discriminatory value for distinguishing between viral and bacterial infections, and results can be obtained in hours or less. In patients with community-acquired pneumonia, procalcitonin is about 65 to 70 percent accurate in distinguishing bacterial from viral pathogen) , INR(An elevated international normalized ratio (INR) has been associated with more severe illness. This finding may herald the development of disseminated intravascular coagulation), blood sugar (Infection causes a stress response in the body by increasing the amount of certain hormones such as cortisol and adrenaline. These hormones work against the action of insulin and, as a result, the body’s production of glucose increases, which results in high blood sugar levels.)
The presence of three of what criteria warrants ICU/HDU admission for pneumonia
Altered mental status
Hypotension requiring fluid support
Temperature less that 36 degrees
Respiratory rate more than or equal to 30cpm
Arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) ratio
Less than or equal to 250
Blood urea nitrogen more than or equal to 20mg/dL(7mmol/L)
Leukocyte count less than 4000cells per
Microlitre
Platelet count less than 100,000/mL
Multilobar infiltrates
What drugs for treatment do you give for out patients with pneumonia and for how long?
How do you treat out patients with comorbidities such as chronic heart, lung, liver, kidney disease,alcohol dependence, or immunosuppression)?l for pneumonia?
Amoxicillin 1g 8 hourly
or
Amoxicillin + Clavulanic acid 625mg 8hrly
Plus or minus Azithromycin 500mg daily
Treat for 5-7 days
Those with comorbidities,
Amoxicillin + Clavulanic acid 1g 12hrly
Or
Cefuroxime 500mg 12hrly
Plus Azithromycin 500mg daily
What drugs for treatment do you give for in patients with pneumonia and for how long?
When do you start treatment ?
If patient has sepsis, when do you start treatment ?
What type of antibiotic is a macrolide
Combination therapy with IV beta-lactam plus a macrolide (Macrolides are a class of drugs used to manage and treat various bacterial infections. Azithromycin, clarithromycin, and erythromycin . macrolide antibiotics are active mainly against Gram‐positive bacteria and have only limited activity against Gram‐negative bacteria. Azithromycin is the macrolide with the best Gram-negative activity of the group and is effective against Shigella and Salmonella species. )
example IV amoxiclav plus Azithromycin /clarithromycin
You may consider a respiratory fluoroquinolone mono therapy
Start treatment within 4 hours of presentation
If patient has sepsis, start treatment within one hour presentation
Treat for 5-7days unless lab results indicate a longer course or patient isn’t clinically stable
What are beta lactams
Beta-lactam antibiotics include penicillins, cephalosporins and related compounds. As a group, these drugs are active against many gram-positive, gram-negative and anaerobic organisms
β-lactam antibiotics are antibiotics that contain a beta-lactam ring in their chemical structure. This includes penicillin derivatives, cephalosporins and cephamycins, monobactams, carbapenems and carbacephems
Apart from drug treatment, what additional management is given to pneumonia patients
When will you give oxygen
Switch to pathogen specific target antibiotic therapy
Oxygen therapy
-prescribe oxygen if saturation is less than 94% and maintain a target range
-a lower target range of 88-92% is appropriate if patient is at risk of being hypercapneic respiratory failure example COPD PATIENTS
-monitor ABGs
Fluid resuscitation
-assess all patients for volume depletion and give IV fluids if required if required
Vasopressors
-start if patient is hypotensive during or after fluid resuscitation to maintain MAP more than or equal to 65mmHg
Venous thromboembolism (VTE) prophylaxis
-consider low molecular weight unfractionated heparin for patients who are not fully mobile
Nutritional support
-arrange nutritional support ( example via nasogastric feeding ) for all patients
Analgesia
-give simple analgesia for chest pain
State six pointers that show that the person is jmproving while on treatment for the pneumonia
Pulse is less than 100 bpm
Resolution of tachypnea
Clinically hydrated and taking oral fluids
Resolution of fever for more than 24hours
Resolution of hypotension
Absence of hypoxia
Imrpoving WBC count
Lack of bacteremia
If initial empirical therapy fails, what do you do next?( for low severity, moderate severity,high severity)
When a Chnage in empirical antibiotic therapy is considered necessary, a macrolide should be substituted for or added to the treatment for those with low severity pneumonia treated with amoxicillin mono therapy in the community or hospitals
For those with moderately severe pneumonia in hospital on combination therapy, changin to doxycycline or a fluoroquinolone with effective pneumococcal cover are alternative options
Adding a fluoroquinolone is an option for those with high severity pneumonia not responding to beta lactam / macrolide combination antibiotic regimen
Consider referral to higher CENTRE with details of management until time of referral
State six complications of pneumonia
Progression of initial infection-sepsis , overwhelming infections
Development of comorbidities and complications (PE,ACS,ARDS)
Pneumothorax
A non resolving infection
-delayed clinical response : extend the treatment to 8-14 days
-loculated infection( this will require drainage )
-incorrect initial diagnosis( consider TB, malignancy, inflammatory lung disease )?
- ineffective antibiotics(example poor absorption or inadequate dose )
- improvement expected too soon
Acronym SLAPHER
S-septicaemia
L-lung abscess
A-ARDS
P-para pneumonic effusion(A parapneumonic effusion refers to the accumulation of fluid in the pleural space in the setting of an adjacent pneumonia. )
H-hypotension
E-empyema (Empyema is defined by purulent fluid collection in the pleural space, which is most commonly caused by pneumonia. A lung abscess, on the other hand, is a parenchymal necrosis with confined cavitation that results from a pulmonary infection.)
R-respiratort failure or renak failure
treptococcus pneumonia is a common etiology of pneumonia with sepsis and, in its acute stage, can increase the risk of AKI. Sepsis-mediated hypoperfusion and hypoxemia may result in peritubular hypoxia and then cause AKI
State six prognosis for pneumonia
-out patients generally have good prognosis
-mortality ranges from five to ten percent in people admitted to the medical ward
Mortality rises to 20-50% in patients in the ICU
Risk factors associated with increased 30day mortality:
-bacteremia
-admission to the ICU
-comorbidities
-infection with multi drug resistant pathogen
Readmission rates ranges from 7-12%
When will you diagnose a COVID 19 patient with mild disease, moderate disease and severe disease
Mild-fever , symptoms of upper respiratory tract infections
SPO2 more than or equal to 97% on room air
Modern-
Symptoms of pneumonia with respiratory rate more than ir equal to 24 cpm
SPO2 less than or equal to 94% on room air
Severe
Respiratory distress requiring Mechanical ventilation( non invasive or invasive )
SPO2 less than or equal to 90% on room air
How will you treat someone diagnosed with COVID 19
mild disease, moderate disease and severe disease
Mild-
Home isolation
Monitoring
Symptom management and supportive care
Antipyretic and analgesic
Moderate:
Home isolation
Monitoring
Symptom management and supportive care
Antipyretic and analgesic
Antibiotic
Monoclonal antibody
Antibiral medication example remdesivir
Severe:
Hospital/ICU admissions
Consider oxygen therapy
Venous thromboembolism prophylaxis
Symptom management and supportive care
Antipyretic and analgesic
Antibiotic
Corticosteroids
Monoclonal antibody
Antibiral medication example remdesivir
Others: IL-6 inhibitor, JAK inhibitor
Explain CURB-65 and what it’s used for
(Mnemonic CURB)
The severity of the illness is a key factor in the decision for admission, and the choice of first or second-line treatment.
— Pneumonia —
C-confusion
U- blood urea nitrogen
R respiratory rate
B- BP
65 patients more than or equal to age 65
Box 8-1: Severity score for community acquired pneumonia (CURB-65)
Severity score may be based on the following, assigning one point to each of the following factors (maximum 5 points);
y Confusion, restlessness, or excessive drowsiness
y Blood Urea Nitrogen ( > 7 mmol/L)
y Respiratory rate ( ≥ 30 per minute in adults, and ≥ 50 in children)
y Low BP (Systolic BP < 90 and/or diastolic BP < 60 mmHg)
y Patients at the extremes of age, (< 5yr or ≥ 65yr)
Interpretation
0-1; consider home treatment
2-3; consider short inpatient hospitalisation
> 3; admit and consider intensive care
In the presence any of the following additional factors, all cases of pneumonia would warrant hospitalisation.
Additional factors
y Coexisting diseases such as chronic lung disease, heart failure or renal dis-
ease
y Extensive disease, multiple lobes involved
y Low oxygen saturation SpO2, < 92% on room air y Severe tachycardia
What is sepsis
Life threatening organ dysfunction caused by a dysregulated host response to infection
It is a clinical syndrome that has biological, physiologic and biochemical abnormalities caused by a dysregulated host response to an infection
Sepsis and the inflammatory response that ensues can lead to multiple organ dysfunction syndrome and death
Sepsis exists on a continuum of severity ranging from infection to septic shock which can lead to multiple organ dysfunction syndrome and death
State and explain the ways sepsis is detected early
How is MAP calculated
Using the QSOFA score
The SOFA score
The adapted NEWS tool
QSOFA-
Quick sequential organ failure assessment score
Low blood pressure less than or equal to 100mmHg
Respiratory rate more than or equal to 22cpm
Altered mental (GCS less than or equal to 14)
Each point is 1
2-3 points means high risk
0-1 point means not high risk
SOFA-
PaO2/FiO2 ratio:0-PaO2/FiO2 more than 400 and a SPO2/FiO2 more than 302
1-PaO2/FiO2 less than 400 and a SPO2/FiO2 less than 302
2-PaO2/FiO2 less than 300 and a SPO2/FiO2 less than 221
3-PaO2/FiO2 Less than 200 and a SPO2/FiO2 Less than 142
4-PaO2/FiO2 Less than 100 and a SPO2/FiO2 Less than 67
Bilirubin(mg/dL): (0) less than 1.2,(1) 1.2-1.9, (2) 2.0-5.9, (3) 6.0-11.9, (4) more than 12
Platelet count(for coagulation. Platelets x10 to the power 3 /mm to the power 3):
(0) more than or equal to 150, (1)les than 150, (2) less than 100, (3) less than 50 , (4) less than 20
Serum creatinine or urine output(for renal mg/dL) :
(0) less than 1.2, (1)1.2-1.9, (2) 2.0-3.4, (3) 3.5-4.9, (4) more than 5.0
Mean arterial pressure (MAP)( doses in mcg/kg/min , Administration of vasopressors and dose rate ,cardiovascular):
(0) MAP more than or equal to 70mmHg, (1) MAP more than or equal to 70mmHg, (2) dopamine less than or equal to 5 or any dobutamine, (3) dopamine more than 5..norepinephrine less than or equal to 0.1…phenylephrine less than or equal to 0.8
(4) dopamine more than 15…norepinephrine more than 0.1…phenylephrine more than 0.8
(Neurological)Glasgow Coma Scale (GCS) score:
(0) 15, (1) 13-14, (2) 10-12, (3)6-9, (4) less than 6
MAP = DP + 1/3(SP – DP)
State six risk factors for sepsis
Bacteremia
advance age more than or equal to 65
Immunosuppression
Diabetes and obesity
Cancer
Previous hospitalization
Community acquired pneumonia
ICU admission
How will someone with sepsis with signs of end organ perfusion present with
Warm flushed skin is present in the early phases of sepsis
As sepsis progresses to shock, the skin may become cool due to redirection of blood flow to core organs
Decreased capillary refill or peripheral cyanosis may indicate shock
Additional signs of hypo perfusion include altered mental status, obtundation or restlessness, oliguria and Anuria
Ileus or absent bowel sounds are often an end stage sign of hypo perfusion
State five tests you’ll do for someone with sepsis and what you expect to see in those tests
Leukocytosis (WBC more than 12 x 10 to the power 9 /L or leukopenia ( WBC less than 4 x 10 to the power 9/L
Normal WBC count with greater than 10 percent immature forms ( left shift)
Hyperglycemia ( plasma glucose more than 140mg/dL or 7.7mmol/L ) in the absence of diabetes
Plasma C reactive protein elevation
Acute oliguria ( urine output less than 0.5mls/kg/hr for at least 2 hours despite adequate fluid resuscitation)
Creatinine increase more than 0.5mg/dL or 44.2 micromol/L
What are the steps to immediate management of sepsis
Read more about them from the slides
Stabilize respiration
Venous access
Fluid resuscitation ( start within 1 hour)
IV antibiotics(start within one hour)
State five things to monitor while treating someon w sepsis
Clinical response ( resolution of confusion , obtundation)
Respiratory improvement (by normalization of RR)
Haemodynamic response (BP resolution, urine output improvement)
Lab parameter response (WBC,CRP , lactate)
Microbiology response (example urinalysis improvement in leukocytes and proteins)
State ten supportive therapies to do while treating septic patient
Blood product infusion
Nutrition
Stress ulcer prophylaxis
Venous thromboembolism
Insulin therapy
External cooling or antipyretics
Mechanical ventilation
Pathophysiology of clubbing
Finger clubbing is the swelling and widening of the fingers and nails, which results from changes in the tissues beneath the nails. While the exact mechanism behind finger clubbing is not yet fully understood, several theories have been proposed.
One of the most widely accepted theories suggests that finger clubbing occurs due to reduced oxygen levels in the blood. When there is a lack of oxygen in the blood, the body’s tissues may release chemicals that promote the growth of blood vessels in the fingers and nails. These new blood vessels can cause the tissues beneath the nails to expand, leading to the characteristic appearance of clubbed fingers.
Another theory suggests that finger clubbing is caused by an increase in the levels of a hormone-like substance called prostaglandin E. Prostaglandin E is involved in inflammation and is produced in response to tissue damage or infections. It may also promote the growth of blood vessels and contribute to the development of finger clubbing.
Various medical conditions can cause finger clubbing. These conditions include lung diseases such as cystic fibrosis, lung cancer, and bronchiectasis. Heart disorders, such as congenital heart disease and endocarditis, can also cause finger clubbing. Additionally, gastrointestinal conditions such as inflammatory bowel disease and liver cirrhosis have been linked to finger clubbing.
In summary, finger clubbing is a complex process that involves changes in the tissues beneath the nails, which can occur due to reduced oxygen levels in the blood, an increase in prostaglandin E levels, or various underlying medical conditions.
