1. Normal pH, serum bicarbonate, and Pco2 levels do not necessarily exclude acid-base disorders. Final pH level is determined by the ratio of bicarbonate and Pco2. The terms “acidemia” and “alkalemia” represent only changes in pH, whereas the terms “acidosis” and “alkalosis” denote underlying pathological processes. Acidosis without acidemia and alkalosis without alkalemia can be seen. Remember to draw blood simultaneously for arterial blood gas measurement and for basic metabolic profile to ensure proper interpretation of acid-base disorders.
2. Always calculate the serum anion gap (AG); otherwise, acid-base disorders may go unrecognized. When calculating AG, pay attention to serum albumin values, which will influence AG significantly. For every 1 g/dL decline in serum albumin <4.4 g/dL, a 2.5 mEq/L reduction in AG occurs. In the case of increased AG, the ratio of AG and HCO3— should be calculated (Δ:Δ). The Δ:Δ<1 suggests mixed normal AG and high AG acidosis; Δ:Δ>2 suggests coexisting metabolic alkalosis. Increases in AG can be seen in nonacidotic states, such as metabolic alkalosis and respiratory alkalosis; however, increases in AG beyond 3 to 5 mEq/L are unusual.
3. Check for appropriate compensation to detect occult mixed acid-base disorders. Over- or undercompensation does not occur and is only indicative of another primary acid-base disorder. Any combination of acid-base disorder can occur, except for respiratory acidosis and respiratory alkalosis. In mixed acid-base disorders, therapeutic decisions should be based on the pH level.
4. Compensation formulas include:Expected compensation in metabolic acidosis:
Pco2 = 1.5 x HCO3— + 8 ±2
Expected compensation in metabolic alkalosis:
Pco2 = 0.6 x ΔHCO3—
Acute respiratory acidosis: ΔHCO3— = 0.1 x ΔPco2
Acute respiratory alkalosis: ΔHCO3— = 0.2 x ΔPco2
Chronic respiratory acidosis: ΔHCO3— = 0.35 x ΔPco2
Chronic respiratory alkalosis: ΔHCO3— = 0.4 x ΔPco2
Since you have to remember 4 formulas for expected compensatory changes in respiratory disorders, “1-4’’ can be used for quick recall.
5. The urinary AG (UAG) can be useful to differentiate between gastrointestinal (GI) and renal causes of a hyperchloremic metabolic acidosis. A negative UAG suggests GI loss of bicarbonate (eg, diarrhea); a positive UAG suggests impaired renal distal acidification (eg, distal renal tubular acidosis). UAG is not useful in volume depletion with urinary sodium <25 mEq/L.
6. In early stages of chronic kidney disease (glomerular filtration rate [GFR] <40 mL/min), normal AG metabolic acidosis can become evident, and as the disease progresses (GFR <20 mL/min), high AG metabolic acidosis can be seen. Serum bicarbonate <10 mEq/L and AG >20 mEq/L are unusual in renal failure and may be indicative of coexistent pathological processes, such as ketoacidosis or lactic acidosis.
7. Lactic acidosis that exceeds 4 to 5 mmol/L in a patient with acidosis is considered significant. The lactate level can exceed 12 mmol/L during grand mal seizures. Drug-induced lactic acidosis has been seen with metformin, isoniazid, and some antiretroviral agents.
8. In adults, salicylate overdose results in mixed metabolic acidosis and respiratory alkalosis; in children, only metabolic acidosis is seen.
9. Diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, and chronic renal failure—but not acute renal failure—are much more common causes of serum osmolal gap increases than are ethylene glycol or methanol intoxications. Serum osmolal gap can be seen without metabolic acidosis, for example, with isopropyl alcohol or with mannitol.
10. Serum osmolal gap of ≥25 mOsm/kg, in the absence of evident causes, strongly suggests methanol or ethylene glycol intoxication. Prophylactic therapy either with fomepizole or with ethanol can be initiated to prevent the formation of toxic metabolites while laboratory test results are pending. Once parent compounds are metabolized, the osmolal gap will disappear, but an increased AG will remain; hence, a normal osmolal gap does not necessarily exclude ethylene glycol or methanol toxicity.
10 pearls of Acid base
How 'bout a little Lung Pathology
Good evening all! I'm trying to give some quick-hit reading and "to know" for those preparing for USMLE Step 1. This will continue for a couple more weeks. Most of those who will be taking this exam will be completing their preparation during the next 3 weeks and then entering the wards, where I could then become their intern when they rotate through their internal medicine clerkship at the University of Kansas. That is when the fun begins. Right now, it is time to focus on preparing to take THE test that either opens or closes future doors of opportunity. Sadly, this exam does weigh that heavily.
All of you preparing for this exam and have scheduled to take it in the middle to late June should be doing lots and lots of questions from a question bank, such as USMLE world or Kaplan. I would also recommend as you go back through your question bank to have your FirstAid book handy and write in the margins those explanations that really make it stick for you.
You should have or should be thinking about taking a full, mock exam. This will build your stamina for THE day and make you work that recall muscle I blogged about earlier this month.
Build your confidence, daily! Know you are in the right place, at the right time to do well.
Make sure you are exercising and eating right.
Make a plan, do your plan, believe in your plan and execute!
Alright... enough soap box stuff. As important as it is, here is some lung path to work your brain over.
Make sure to inhale! ;)
Interstitial Lung Diseases
Acute Lung Injury- rapid onset, short duration
- Diffuse Alveolar Damage (DAD)- specific cause, rapid progression-infiltrates
- Acute Interstitial Pneumonia (hamman-rich disease)- like DAD, only no specific cause, fulminant course- need biopsy
o The above two present with pretty severe respiratory symptoms
- Bronchiolitis Obliterans (BOOP)- only one with a good prognosis, air space disease- fibroid polyps filling airspaces
o Presents with fever, cough, dyspnea, bilateral infiltrates
Chronic Interstitial Pneumonia
- Usual Interstitial Pneumonia- varying histology- fibrosis, inflammation
o Infiltrates periphery, base
o Worse prognosis, older people 55
- Desquamative Interstitial Pneumonia- uniform, macrophages in airspace
o Better prognosis---younger 45
Honeycomb lung- dilation/mucous filling air spaces/cyst formation/obliteration of small airspaces to create big ones---end stage
- Acute lung injury- DAD
- Chronic- BOTH UIP, DIP
- Asbestos
- Interstitial glanulomatous diseases
- Eosinophillic granuloma
Hypersensitivity Pneumonitis= Extrinsic Allergic Alveolitis
Non-Necrotizing Granuloma: Hypersensitivity Pneumonitis
Necrotizing Granuloma: Wegener's granulomatosis
Cyclophosphamide
- UIP
- Wegener's Granulamatosis
Diffuse Pulmonary Hemorrhage Syndromes
- Goodpasture's Syndrome---young males, kidney too
o Hemorrhage in intraalveolar spaces
- Vasculitis assoc- both have good prognosis with treatment
o Wegener's granulomatosis-- 50 y/o males, kidney too--mostly other organs
Necrotizing granuloma in lung and vasculature (necrotizing vasculitis)
C-ANCA
o Chrug-Strauss- ASTHMA, P-ANCA, RARE kidney: skin, nerves, heart, looks like eosinophilic pneumonia
Pulmonary Eosinophilia
- eosinophills in BLOOD or SPUTUM…NOT IN LUNG TISSUE ITSELF
- DISEASES:
o Churg-strauss (see above)
o Eosinophilic pneumonias
Simple- LOEFFLER'S SYNDROME- transient infiltrates
Tropical- filiarial
Chronic- only one that needs biopsy, assoc w/ASTHMA
• Responds well to steroids, lots of diff causes
o Allergic bronchopulmonary aspergilliosis- NO BIOPSY
Hypersens to aspergillius (acute branching hyphae)
Ab to aspergillius, central bronchiectasis (dilation)
Immune, not infectious- treat w/ steroids
Pulmonary Eosinophilic Granuloma (histiocytosis X)
- is NOT A PULMONARY EOSINOPHILIA!!!!!!!!
- the eosinophils are located in the lung tissue, NOT the peripheral blood/sputum
- histocyte proliferation, with a pneumothorax (air in pleural cavity)
- langerhans cells w/ bierbeck granule(ovoid nucleus with central line, stain with S-100) CD 1+
- treatment: stop smoking, corticosteroids
Diseases associated with ASTHMATICS- all have pulmonary eosinophilia (makes sense)
- Churg-Strauss
- Chronic eosinophilic pneumonia
- Allergic bronchopulmonary aspergilliosis
Immunologic lung diseases
- Goodpastures
- Allergic bronchopulm aspergilliosis
Sarcoidiosis- multisystem granulomatosis disease
- multiple non caseating, non necrotizing granulomas, usu along lymph pathways (different from TB- which would caseate)
- black, female, 20-40 y/o
- bilateral infiltrates, hilar lymphadenopathy
- increased serum angiotensin converting enzyme
- increased 24 hour calcium secretion
Necrotizing Granulomas along blood pathways- Wegener's granulomatosis
Non-necrotizing granulomas along lymph pathways- sarcoidiosis
Pneumonconiosis
- non-neoplastic rxn in lung to inhaled mineral/organic dust
- Asbestos Diseases
o Asbestosis- pulmonary parenchymal interstitital fibrosis
o Pleural plaque
o Pleural effusion
o Bronchogenic carcinoma
o Malignant mesothelioma
o Laryngeal/extrapulmonary neoplasms
Lung Biopsies
- OLB- gold standard
- VALB- not good for central biopsy
- TBB- good for sarcoid, cancer, infections
o Bad for UIP, DIP
COPD/PFT
Chronic Obstructive Diseases
- Chronic Bronchitis
- Emphysema
o Above two are usually considered COPD
- Asthma
- Bronchiectasis
Chronic Bronchitis
- middle ages, smokers, males
- hallmarks:
o hypertrophy/hyperplasia of submucosal glands (ried Index)
RIED index- meas ratio of submucosal gland thickness to thickness of bronchial wall..>0.4 is bad
o goblet cell metaplasia in bronchi
Remember----terminal bronchiole---respiratory bronchiole---alveolus
Emphysema: enlargement of airspaces, distal to terminal bronchiole
- pathogenesis: protease/antiprotease balance
- defined in morphologic terms
- males, smoking, 50-80 y/o
Types
- centrilobular: most common, resp bronchioles, UPPER lobes
- panlobular: involves BOTH resp bronch and alveoli (whole acinus), LOWER lobes
o alpha-1-antitrypsin defiency (PiZZ genotype)
- localized - (paraseptal), enlargement distal acinus, upper lung, usu asymptomatic
o young adults- spontaneous pneumothorax
- Irregular (paracicatricial emphysema)- fibrosis
- Bullous- occurs w/ other emphysemas
Asthma:
- smooth musc contraction, mucous secretion, increased vascular permeability-edema---leads to bronchial obstruction
- thickened bronchial basement membrane of bronchioles, hypertrophy of bronchial smooth muscle, mucous plugs
Bronchiectasis
- irreversible dilation of bronchi- due to elastic/muscular elements in wall
- Immotile cilia syndrome
o Inherited non-obstructive cause
o Includes Kartagener syndrome: dextrocardia, bronchiectasis, sinusitis, rhinitis, nasal polyps, otitis media
Non Productive cough: Asthma
Productive Cough: bronchiectasis (mucopurulent sputum)
Middle Aged men
- UIP
- DIP
- Hypersensitivity pneumonia
Pulmonary fxn tests
- when have pulmonary function tests: the percent predicted is the "percentage that the "ideal" predicted value that the patient has achieved
- Forced Expiratory Flow :slope of line through volume/time graphs
o FEF 25-75%- small airway disease
o FEF 200-1200- large airway disease
Infectious Lung Diseases
Productive Cough: Bacterial Pneumonia
Bacterial Pneumonia
- Community Acquired Pneumonia: mild- bad if co-morbidities
- Nosocomial
- Opportunistic
- Abscess is complication of bacterial pneumonia
Viral Pneumonia: usu kids, immunocomp
- chronic interstitial pneumonia- lymphocytes
- diffuse alveolar damage- hyaline membranes
- Cytomegalovirus
o Immunocomp,
o Fever, non productive cough, diffuse infiltrates
o Intranuclear inclusion bodies, intracytoplasmic inclusions
Pneumocystis Pneumonia
- immuno comp
- fever, dry cough,
- inter-alveolar FOAMY exudates
Pulmonary Fungal Infections
- Histoplasmosis
o Soil, bird/bat droppings
o Granulomatous inflammation, small black budding yeast
- Coccidiodomycosis
o Southwest
o Necrotizing granulomatous inflammation
- Cryptococcosis - india ink stain
o Soil, PIGEON poop
o Mucin positive
- North american blastomycosis
o mid west river valleys
o pus forming (suppurative)/granulomatous
o BROAD based budding
- Aspergillosis
o Allergic bronchopulmonary aspergillosis- immunologic
o Aspergilloma- colonizes pulmonary cavity- fungus ball
o Invasive aspergillosis- opportunistic infection
Vascular invasion, thrombus + infarct
Can see hyphae and fruiting bodies
Tuburculosis
- Gohn complex: peripheral granuloma, involvement w/ mediastinal lymph node
Stuff that forms Granulomas
Necrotizing
- TB
- Coccidiomycosis
Non-Necrotizing
Lung Cancer
Men, 60-70 y/o
Central Tumors
- small cell carcinoma
- squamous cell carcinoma
- branchial carcinoids
Peripheral Tumor
- adenocarcinoma
- hamartoma
Malignant
Epithelial Tumors
- squamous cell carcinoma
o smoking males, central lung- keratin pearls
o hemotypsis, symp due to obstruction
o superior vena cava syndrome- compression, dilation of upper body veins
o pancoast syndrome- shoulder pain- ulnar distribution: b/c tumor at apex compresses parts of brachial plexis
o Horner syndrome- b/c pancoast tumor that involves cervical symp plexus- ptosis, miosis, anhydrosis, endopthalmosis
o Massive hemorrhage, dilated bronchi mucopurulent secretions,
o 5 years, 15%
- adenocarcinoma
o peripheral, assoc with scars
o 5 year 15-20%
o Types
Acinar adenocarcinoma
• Gland arrangement, mucous secretions
Broncho-alveolar carcinoma
• Male female 1:1, 5 year 42%, multicentric/diffuse forms worse
• Neoplastic cells line "normal" alveolar architecture
• Types
o Solitary mass
o Multiple nodules- resembles metastatic cancer
o Multicentric diffuse infiltrate- resembles interstitial disease
Solid carcinoma w/ mucous cell formation
• Undifferentiated, anaplastic
Papillary adenocarcinoma
• Papillary structures with central fibrovascular core
Neuroendocrine Carcinomas (small and large cell carcinomas): acts like neuroendocrine system
Small cell carcinoma
o Males, smoking
o Worst prognosis 5 yr 4%, already metastatic by time of diagnosis
o Best response to cancer- important to ID as small cell for TX
o Central
o Types
Oat Cell
Intermediate
• Similar clinically
Combined- oat cell + any other type of tumor (squamous or adenoma)
• Perform surgery to remove
- Large cell carcinoma
o Poorly differentiated- no observable org via light microscopy
Electron microcsopy shows some organization
o cells with lots of cytoplasm (+ lymphocytes…not oat cells)
o Treat with SURGERY NOT CHEMO
Bronchial Carcinoids
- M=F, 45 y/o
- Central, peripheral, atypical
- Central
o GOOD PROGNOSIS- 5-10 y 50-95%!
o Maj metast to lymph, minor to liver
o YELLOWISH color
o Mass invading lumen of larger bronchi (more central)
o Invade bronchial wall into lung tissue
o Uniform cells, strippled chromatin, positive stain for chromogranin
o Can UNUSUALLY cause carcinoid syndrome (via seretonin secretion- skin flush, broncho const, cyanosis, R heart prob, hypotension,edema)
Metastatic Tumors
- lung 2nd most freq after lymph node
- Types
o Multiple- usu late stage cancers
o Lymphangitic- usu from adenocarcinoma
o Solitary- must distinguish from primary tumor
- usu from stomach, breast, colon, uterus, pancreas
Malignant Mesothelioma
- males, 40-70 y/o
- increasing in freq
- asbestos exposure (20-40 year lag)
- PLEURAL EFFUSION
- Pleural tumor encasing the lung- can extend to diaphragm
- Biphasic: epithelial/spindle
Benign
Hamartoma
- Peripheral, well defined
- hamartoma means like tumor, but due to faulty development
o microscopically can reproduce any component of bronchial tissue- cartilage, muscle, fat, cleft like spaces
Putting it all together….
Small cell carcinoma: major one for chemo
All other tumors- surgery is treatment of choice!!
Overall cancer survival rate: 5 years, 8-10 %
In order of better to worse
- squamous, adeno, small, large
Squamous cell, adeno= better prog
Small/Large cell= bad prog
Metastasis: most likely to least likely: lymph nodes, liver, adrenal, bone, brain
Paraneoplastic syndromes
Squamous cell carcinoma: hypercalcemia- PTH
Small cell carcinoma: cushing's (ACTH), inapprop ADH, carcinoid, gyneocmastia, acromegaly
Squamous cell and adenocarcinoma ( prob most frequent and increasing!)are most frequent lung tumors
- small cell and large cell also considered frequent
Drugs with Lung Toxicity:
Bleomycin
Busulfan
Amiodarone
Cyclophosphamide
Methotrexate and methysergide
Nitrosourea and nitrofurantoin
Virus Thoughts: 2009: H1N1
All the recent talk about a possible pandemic have caused quite a stir. It is yet to be determined whether this will be more serious but here is some info concerning the this virus. Food for thought (no pun intended)
Orthomyxovirus (Ordinary flu)
The new HA and NA antigens are given number subscripts to differntiate them. the pandemic of 1889 was caused by a virus with an H2 hemagglutinin, the pandemic of 1900 was caused by a new virus with H3 hemagglutinin; in 1918, a swine flu virus transferred its HA to a human virus and so was called Hswine hemagglutinin (HSW). The chart below is only included to demonstrate the many pandemics and their new HA and NA antigenic composition
Global Pandemics:
1889: H2N2
1900: H3N2
1918: H1N1 - "Spanish flu" - highly pathogenic stgrain - with high mortality
(est. 20-40 million deaths worldwide).
1947: H1N1*
1957: H2N2* "Asian Flu" - illness, but low mortality
1968: H3N2* "Hong Kong flu" - illness, but low mortality
1977: H1N1*
* Notice also tha.t some strains caused a second pandemic as a new unexposed population grows to adulthood
Will the next pandemic post be, 2009: H1N1 - swine flu?
Very important to remember!! Never give children with influenza or varicella (chicken pox) aspirin. Reye's Syndrome - Severe Liver and brain disease. It is not yet known why it occurs.
Trepidation and new beginnings
Starting any new adventure is a time of trepidation. The trepidation is buffered with an excitement and energy that keeps the fears, mostly, at bay.
The previous four years have enabled me to become a physician, yet somehow, I am anxious about the process I will endure in my internship (and the next year in my 1st year of residency as an Anesthesiologist). I think that I am ready, yet I know I am unprepared at the same time. I know there will be many times I feel completely fulfilled and others where I know I have yet to learn what I should already know. I do know I am ready to complete the process and excited to learn.
In the mean time, I will be helping prepare 2nd year medical students for their USMLE Step 1 exam. This is arguably the most important exam of their career and one which causes great 'trepidation' to many a 2nd year medical student. I feel their pain, yet know they will do fine, IF they listen to me (haaaaaaaaaa!). I will be apart of The University of Kansas' Step Prep Program. This program is designed to give 2nd year medical students some basic tools to maximize their potential score on THE exam. I am part of a 3 person team that will facilitate them, coach them, and encourage them in this process. There will be approx. 10 teams with 8-10 students/group.
Over the next month, this blog will, hopefully, pass along some of those pearls and encourage you to reach your best. Check back here soon and I will be posting questions, pearls, mneumonics, links and other such info you might want to know.
Good luck!