Metabolic Superstorm
1. Fill in the chart below. Use “+” if the patient’s vital sign is higher than normal, “−” if the sign is lower than normal, or “x” if the sign is normal. If you need to, use your text or another resource to determine normal values.
Vital Sign Increase/Decrease/Normal
Respiration Rate +
Heart Rate +
Blood Pressure -
Body Temperature +
2. If you were the doctors on the scene, what diagnosis would you give this patient? (You may use the internet to help diagnose the patient.)
I would question as to whether he has any allergies. The heart rate and respiration elevation, and low blood pressure can be present in allergic reactions.
3. Jot down some notes about your
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- ATP hydrolysis – myosin head swings and binds to a new actin - Release of Pi initiates the power stroke Steps that require Ca24: release of Ca from the cisternae of the sarcoplasmic reticulum
Ca binds to troponin
Assignment 3
1. Predict if healthy muscle or muscle with MH will contract with the most force. The MH muscles generates excessive contraction.
3. Even though screening tests exist, most people aren’t checked for the disease. Why not?
What types of people (or what populations) would be most likely to be screened before they had their first surgery?
The testing takes time, and often people need to be admitted for surgeries quickly. Cost may also be a prohibitive factor for the poor or elderly.
Assignment 4
2) Answers to Emily’s questions:
1) How do muscles contract?
-Action potential arrives at axon terminal of motor neuron;
-Acetylcholine (ACh) is released and binds to receptors on sarcolemma;
-The sarcolemma’s Ion permeability changes;
-depolarization occurs locally in the sarcolemma;
-This local change in membrane voltage ignites Action Potential in sarcolemma;
-Action Potential travels across the entire sarcolemma and along the T tubules;
-Sarcoplasmic Reticulum (SR) then releases Calcium which binds to troponin in the thin filament, exposing myosin-binding sites;
-Myosin heads bind to actin causing
tells you that he began feeling changes in his heart rhythm about 10 days ago. He has hypertension
This activity is the critical driving force of muscle contraction. The stream of action potentials along the muscle fiber surface is terminated as Acetylcholine at the neuromuscular junction is broken down by acetyl cholinesterase. The release of Calcium ions is ceased. The action of the myosin molecule heads is obstructed because of the change in the configuration of troponin and tropomyosin due to the absence of calcium ions. This will eventually cause the contraction to be ceased. Together with these physical processes, an external stretching force such as gravity pulls the muscle back to its normal length.
Physical Examination: General: The patient is an alert, oriented male appearing his stated age. He appears to be in moderate distress. Vital signs: blood pressure 132/78 and pulse 68 and regular. Temperature is 38.56 oC (101.4 oF). HEENT:Normocephalic, atraumatic. Pupils were equal, round, and reactive to light. Ears are clear. Throat is normal. Neck: The neck is supple with no carotid bruits. Lungs: The lungs are clear to auscultation and percussion. Heart: Regular rate and rhythm. Abdomen:Bowel sounds are normal. There is rebound tenderness with maximal discomfort on palpation in the right lower quadrant. Extremities: No clubbing, cyanosis, or edema.
muscular rigidity. Explain why a lack of ATP would cause the sustained muscle contraction of rigor mortis.
Smooth muscle contraction occurs when calcium is present in the smooth muscle cell and binds onto calmodulin to activate myosin light chain kinase (Wilson et al., 2002). Phosphorylation of myosin light chains result in myosin ATPase activity thus cross-bridge cycling occurs causing the muscle to contract (Horowitz et al., 1996). There are two known models of excitation and contraction in smooth muscle, electromechanical coupling (EMC) and pharmomechanical coupling
1. Weeding out misinformation and piecing together the many facts presented, what is your diagnosis of Joe’s condition?
As Jane was presenting with a symptom of a life threatening event it was important that treatment was immediate. Priority was initially made from assessment of the airways, breathing and circulation, level of consciousness and pain. Jane’s respirations on admission were recorded at a rate of 28 breaths per minute, she looked cyanosed. Jane’s other clinical observations recorded a heart rate of 105 beats per minute (sinus tachycardia), blood pressure (BP) of 140/85 and oxygen saturation (SPO2) on room air 87%. It is important to establish a base line so that the nurse is altered to sudden deterioration in the patient’s clinical condition. Jane’s PEWS score (Physiological Early Warning Score) was 4 and indicated a need for urgent medical attention (BTS 2006). Breathing was the most obvious issue and was the immediate priority.
hypotensive with a blood pressure of 82/44 mm Hg. His respiratory rate is 28 breaths/min
Pulse rate is at 72. The blood pressure was 140 / 95,which is suggestive of high blood pressure and related to his medical history. No heart murmur was noted, and no other abnormalities were noted.
Early detection, screening and prevention, often times is not provided by mainstream America to support programs that benefit all American’s. Often Minority groups are sometimes five years after preventative screening before tests are available to
Screening tests are only available through biopsies. This means that basically once symptoms arise, one would be able to go and get a prognosis as to whether or not they have this disease.
States that it started 3 days back and uses oxygen at home. States that he is a former smoker and laying on his back feels better. Also says he has a list of medication, more than 20. Pt has a history of COPD, CHF, DM,morbid obesity, HTN, HLM, hypothyroid, and sleep apnea. Has no accessory muscle use. CC is shortness of breath. Assessment is that there is no deformities or trauma of the head or neck area. Chest shows no signs of deformities or trauma. The abdominal area is tender and warm to the touch. Pelvis and back was not assessed. The upper and lower extremities show signs of low circulation and swelling. PMS=4. I helped with placing the BP cuff on the left arm and attaching it to the monitor. First vitals were recorded. O2 was given by the Nurse and then Albuterol by nebulizer. After 30 minutes, I assisted the Nurse and other hospital workers in moving the PT to a bigger bed. Second set of vitals were recorded. After becoming stable the Pt was moved up to the floor.
Hypertension. His blood pressure is great here in the office. I will have him continue with his same medication and I will continue to follow along and he was asked also monitor for signs of hypotension and I did review with him what to be monitoring for.
Myofibrils are made up of long proteins that include myosin, titin, and actin while other proteins bind them together. These proteins are arranged into thin and thick filaments that are repetitive along the myofibril in sectors known as sarcomeres. The sliding of actin and myosin filaments along each other is when the muscle is contracting. Dark A-bands and light I-bands reappear along myofibrils. The alignment of myofibrils causes an appearance of the cell to look banded or striated. A myofibril is made up of lots of sarcomeres. As the sarcomeres contract individually the muscle cells and myofibrils shorten in length. The longitudinal section of skeletal muscle exhibits a unique pattern of alternating light and dark bands. The dark staining, A-bands possess a pale region in the middle called the H-zone. In the middle of the H-zone the M-line is found, that displays filamentous structures that can join the thick filaments. The light-staining bands also known as I-bands are divided by thin Z-line. These striated patterns appear because of the presence of myofibrils in the sarcoplasm (IUPUI, 2016).